Raynaud's affects parts of the body that have a characteristic circulatory pattern: a high density of direct connections between arterioles — small vessels that branch out from arteries — and venules, or small veins.
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The organoids easily took to their new home, connecting to the mice's native circulatory system, and developed even further into a tree-like network of arteries, small veins, and arterioles (branches of an artery that flow into capillaries).
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When people with Raynaud's are exposed to cold or are under stress, normal nervous system-induced constriction of the arterioles in these anastomoses is enhanced and may temporarily cut off blood flow to the affected parts, causing them to turn white and feel cold and numb.
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The bulbar conjunctival microvasculature contains arterioles, meta-arterioles, venules, capillaries, and communicating vessels. Vessel morphology varies greatly between subjects and even between regions of the individual eyes. In some subjects, arterioles and venules can be seen to run parallel with each other. Paired arterioles are generally smaller than corresponding venules.
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The major determinant of vascular resistance is small arteriolar (known as resistance arterioles) tone. These vessels are from 450 µm down to 100 µm in diameter. (As a comparison, the diameter of a capillary is about 5 to 10 µm.) Another determinant of vascular resistance is the pre- capillary arterioles. These arterioles are less than 100 µm in diameter.
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The afferent arterioles are a group of blood vessels that supply the nephrons in many excretory systems. They play an important role in the regulation of blood pressure as a part of the tubuloglomerular feedback mechanism. The afferent arterioles branch from the renal artery, which supplies blood to the kidneys. The afferent arterioles later diverge into the capillaries of the glomerulus.
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Systemic arteries deliver blood to the arterioles, and then to the capillaries, where nutrients and gases are exchanged. After traveling from the aorta, blood travels through peripheral arteries into smaller arteries called arterioles, and eventually to capillaries. Arterioles help in regulating blood pressure by the variable contraction of the smooth muscle of their walls, and deliver blood to the capillaries.
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Metarterioles connect arterioles and capillaries. A tributary to the venules is known as a thoroughfare channel. The microcirculation has three major components: pre-capillary, capillary, and post-capillary. In the pre-capillary sector, arterioles, and precapillary sphincters participate.
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At the vascular pole, the afferent arterioles and efferent arterioles enter and leave the glomerulus in the Bowman's capsule. The tubular pole is at the other end opposite to the vascular pole. At the tubular pole, the proximal convoluted tubule arises.
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Second, prostaglandin activates prostaglandin-sensitive specialized smooth muscle cells of the renal afferent arterioles, juxtaglomerular cells (JG cells), to release renin into the bloodstream. The JG cells can also release renin independently of the macula densa. There are stretch-sensitive baroreceptors lining the arterioles that will release renin if a fall in blood pressure (i.e. decreased stretch of arteriole due to less blood flow) in the arterioles is detected.
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Metarterioles exist in the mesenteric microcirculation, and the name was originally conceived only to define the "thoroughfare channels " between arterioles and venules. In recent times the term has often been used instead to describe the smallest arterioles directly prior to the capillaries.
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Additionally, vasopressin selectively contracts efferent arterioles probably through the V1R, but not the afferent arteriole.
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Variations in the flow of blood that circulates by arterioles are capable of responses in endothelium.
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Pulmonary arterioles are a noteworthy exception as they vasodilate in response to high oxygen. Brain arterioles are particularly sensitive to pH with reduced pH promoting vasodilation. A number of hormones influence arteriole tone such as angiotensin II (vasoconstrictive), endothelin (vasoconstrictive), bradykinin (vasodilation), atrial natriuretic peptide (vasodilation), and prostacyclin (vasodilation).
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The muscular contraction of arterioles is targeted by drugs that lower blood pressure (antihypertensives), for example the dihydropyridines (nifedipine and nicardipine), which block the calcium conductance in the muscular layer of the arterioles, causing relaxation. This decreases the resistance to flow into peripheral vascular beds, lowering overall systemic pressure.
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The vasa recta of the kidney, (vasa rectae renis) are the straight arterioles, and the straight venules of the kidney, – a series of blood vessels in the blood supply of the kidney that enter the medulla as the straight arterioles, and leave the medulla to ascend to the cortex as the straight venules. (Latin: vasa, "vessels"; recta, "straight"). They lie parallel to the loop of Henle. These vessels branch off the efferent arterioles of juxtamedullary nephrons (those nephrons closest to the medulla).
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The afferent arterioles, then, enter Bowman's capsule and end in the glomerulus. From each glomerulus, the corresponding efferent arteriole arises and then exits the capsule near the point where the afferent arteriole enters. Distally, efferent arterioles branch out to form dense plexuses (i.e., capillary beds) around their adjacent renal tubules.
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Kidneys of common ravens receive arterial and afferent venous blood and are drained by efferent veins. In terms of the arterial blood supply, the arteries entering the kidneys branch into numerous smaller arteries and eventually form afferent arterioles that supply the glomeruli. The peritubular blood supply is composed of efferent arterioles leaving the glomeruli of reptilian-type nephrons that drain into sinuses of the cortex. On the other hand, the vasa recta are formed by efferent arterioles exiting the glomeruli of mammalia-type nephrons.
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The regulation of tissue perfusion occurs in microcirculation. There, arterioles control the flow of blood to the capillaries. Arterioles contract and relax, varying their diameter and vascular tone, as the vascular smooth muscle responds to diverse stimuli. Distension of the vessels due to increased blood pressure is a fundamental stimulus for muscle contraction in arteriolar walls.
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Arteries branch into small passages called arterioles and then into the capillaries. The capillaries merge to bring blood into the venous system.
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Both the short gastric arteries and the splenic artery supply it with blood. The germinal centers are supplied by arterioles called penicilliary radicles.
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Microscopically, the affected nerve is markedly distorted, with extensive concentric perineural fibrosis. The arterioles are thickened and occlusion by thrombi are occasionally present.
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On a histological slide, the straight arterioles can be distinguished from the tubules of the loop of Henle by the presence of blood.
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Similar to the atrium, the arteries are composed of thick elastic muscles to withstand the pressure of the ventricular constriction, and become more rigid as they move away from the heart. Blood moves through the arteries, which undergo vasoconstriction, and into arterioles which act as a transportation system to distribute primarily oxygen as well as nutrients to all tissues of the body. As the arterioles move away from the heart and into individual organs and tissues they are further divided to increase surface area and slow blood flow. Travelling through the arterioles blood moves into the capillaries where gas exchange can occur.
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An arteriole is a small-diameter blood vessel in the microcirculation that extends and branches out from an artery and leads to capillaries. Arterioles have muscular walls (usually only one to two layers of smooth muscle) and are the primary site of vascular resistance. The greatest change in blood pressure and velocity of blood flow occurs at the transition of arterioles to capillaries.
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Diagram of the circulation related to a single glomerulus, associated tubule, and collecting system. The glomerulus receives its blood supply from an afferent arteriole of the renal arterial circulation. Unlike most capillary beds, the glomerular capillaries exit into efferent arterioles rather than venules. The resistance of the efferent arterioles causes sufficient hydrostatic pressure within the glomerulus to provide the force for ultrafiltration.
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The microcirculation is the circulation of the blood in the smallest blood vessels, the microvessels of the microvasculature present within organ tissues. The microvessels include terminal arterioles, metarterioles, capillaries, and venules. Arterioles carry oxygenated blood to the capillaries, and blood flows out of the capillaries through venules into veins. In addition to these blood vessels, the microcirculation also includes lymphatic capillaries and collecting ducts.
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Hill, Richard W. (2012) Animal Physiology/ Richard W. Hill, Gordon A. Wyse, Margaret Anderson. Third Edition pp. 647–678. Sinauer Associates, Sunderland, MA As the arterioles move away from the heart and into individual organs and tissues they are further divided to increase surface area and slow blood flow. Blood travels through the arterioles and moves into the capillaries where gas exchange can occur.
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The glomerulus receives its blood supply from an afferent arteriole of the renal arterial circulation. Unlike most capillary beds, the glomerular capillaries exit into efferent arterioles rather than venules. The resistance of the efferent arterioles causes sufficient hydrostatic pressure within the glomerulus to provide the force for ultrafiltration. The glomerulus and its surrounding Bowman's capsule constitute a renal corpuscle, the basic filtration unit of the kidney.
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In order to understand how blood is delivered to cranial tissues, it is important to understand the vascular anatomy of the space itself. Large cerebral arteries in the brain split into smaller arterioles, also known as pial arteries. These consist of endothelial cells and smooth muscle cells, and as these pial arteries further branch and run deeper into the brain, they associate with glial cells, namely astrocytes. The intracerebral arterioles and capillaries are unlike systemic arterioles and capillaries in that they do not readily allow substances to diffuse through them; they are connected by tight junctions in order to form the blood brain barrier (BBB).
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Pinacidil is a cyanoguanidine drug that opens ATP-sensitive potassium channels producing peripheral vasodilatation of arterioles. It reduces blood pressure and peripheral resistance and produces fluid retention.
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Salus's sign is a clinical sign in which deflection of retinal venules can be seen on fundoscopy occurring in patients with hypertensive retinopathy.Hypertension at Medscape Arteriosclerosis causes shortening or lengthening of arterioles, which causes venules to be moved at points where arterioles and venules cross over. This is seen at right-angle crossing points, where the venule crosses the arteriole in a horseshoe shape.Sebastian Wolf, Berndt Kirchof, Martin Reim.
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The marginal zone (MZ) is a highly transited area that receives large amounts of blood from the general circulation. Remarkably, the splenic microvasculature shows striking differences in mice and humans. In humans, the spleen receives blood from the splenic artery, which branches into central and penicillary arterioles. Owing to the absence of a histologically defined marginal sinus, the blood flowing in penicillary arterioles directly drains into capillaries of the red pulp and perifollicular zone.
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The efferent arterioles are blood vessels that are part of the urinary tract of organisms. Efferent (from Latin ex + ferre) means "outgoing", in this case meaning carrying blood out away from the glomerulus. The efferent arterioles from a convergence of the capillaries of the glomerulus, and carry blood away from the glomerulus that has already been filtered. They play an important role in maintaining the glomerular filtration rate despite fluctuations in blood pressure.
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Conversely, when blood supply to the skin must be reduced these shunts can be closed and furthermore, the normal mechanism of vasoconstriction of arterioles, can dramatically reduce perfusion of the skin.
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The use of countercurrent heat exchange with blood flow allows for regulated conservation/ elimination of heat of appendages. When ambient temperatures are low, heterotherms will constrict their arterioles to reduce heat loss along skin surfaces. The reverse occurs at high ambient temperatures, arterioles dilate to increase heat loss. At ambient temperatures below their body temperatures (thermal neutral zone (TNZ)), common ostriches decrease body surface temperatures so that heat loss occurs only across about 10% of total surface area.
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Arterioles have the greatest collective influence on both local blood flow and on overall blood pressure. They are the primary "adjustable nozzles" in the blood system, across which the greatest pressure drop occurs. The combination of heart output (cardiac output) and systemic vascular resistance, which refers to the collective resistance of all of the body's arterioles, are the principal determinants of arterial blood pressure at any given moment. Arteries have the highest pressure and have narrow lumen diameter.
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Catecholamines (norepinephrine and epinephrine) increase filtration fraction by vasoconstriction of afferent and efferent arterioles, possibly through activation of alpha-1 adrenergic receptors. Severe haemorrhage will also result in an increased filtration fraction.
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The vessels on the arterial side of the microcirculation are called the arterioles, which are well innervated, are surrounded by smooth muscle cells, and are 10-100 μm in diameter. Arterioles carry the blood to the capillaries, which are not innervated, have no smooth muscle, and are about 5-8 μm in diameter. Blood flows out of the capillaries into the venules, which have little smooth muscle and are 10-200 μm. The blood flows from the venules into the veins.
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The vascular amyloid pathology characteristic of CAA can be classified as either Type 1 or Type 2, the latter type being the more common. Type 1 CAA pathology entails detectable amyloid deposits within cortical capillaries as well as within the leptomeningeal and cortical arteries and arterioles. In type 2 CAA pathology, amyloid deposits are present in leptomeningeal and cortical arteries and arterioles, but not in capillaries. Deposits in veins or venules are possible in either type but are far less prevalent.
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Lastly, due to recent experiments, it seems that Nox2 also plays an important role in angiotensin II-mediated inward remodelling in cerebral arterioles due to the emittance of superoxides from Nox2-containing NADPH oxidases.
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Hypertension 6: I75-81. According to the autoregulation breakthrough conception, cerebral arterioles are forced to dilate, leading to vasogenic edema. Cerebral edema can be generalized or focal. Brain ventricles are compressed, cortical gyri flattened.
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Diagram showing the basic physiologic mechanisms of the kidney In renal physiology, ultrafiltration occurs at the barrier between the blood and the filtrate in the glomerular capsule (Bowman's capsule) in the kidneys. As in nonbiological examples of ultrafiltration, pressure (in this case blood pressure) and concentration gradients lead to a separation through a semipermeable membrane (provided by the podocytes). The Bowman's capsule contains a dense capillary network called the glomerulus. Blood flows into these capillaries through the afferent arterioles and leaves through the efferent arterioles.
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Normally, cerebral blood flow is maintained by an autoregulation mechanism that dilates arterioles in response to blood pressure decreases and constricts arterioles in response to blood pressure increases. This autoregulation falters when hypertension becomes excessive. According to the over-regulation conception, brain vessels spasm in response to acute hypertension, which results in cerebral ischemia and cytotoxic edema.Tamaki K, Sadoshima S, Baumbach GL, Iadecola C, Reis DJ, Heistad DD (1984) Evidence that disruption of the blood–brain barrier precedes reduction in cerebral blood flow in hypertensive encephalopathy.
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2006, p. S1 An arteriovenous fistula can increase preload. AV shunts also decrease the afterload of the heart. This is because the blood bypasses the arterioles which results in a decrease in the total peripheral resistance (TPR).
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In 1866 he received his habilitation, and during the following year became an associate professor at Leipzig. His name is associated with "Schweigger-Seidel sheaths", which are spindle-shaped sleeves that cover penicillar arterioles of the spleen.
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This allows arterioles to increase resistance in response to increased blood pressure and thus maintain constant blood flow. The Rhoa and Rac portion of the signaling pathway provides a calcium-independent way to regulate resistance artery tone.
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The juxtaglomerular cells (JG cells, or granular cells) are cells in the kidney that synthesize, store, and secrete the enzyme renin. They are specialized smooth muscle cells mainly in the walls of the afferent arterioles (and some in the efferent arterioles) that deliver blood to the glomerulus. In synthesizing renin, they play a critical role in the renin–angiotensin system and thus in autoregulation of the kidney. Juxtaglomerular cells secrete renin in response to a drop in pressure detected by stretch receptors in the vascular walls, or when stimulated by macula densa cells.
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An increase in the salt concentration causes several cell signals to eventually cause the adjacent afferent arteriole to constrict. This decreases the amount of blood coming from the afferent arterioles to the glomerular capillaries, and therefore decreases the amount of fluid that goes from the glomerular capillaries into the Bowman's space (the glomerular filtration rate (GFR)). When there is a decrease in the sodium concentration, less sodium is reabsorbed in the macular densa cells. The cells increase the production of nitric oxide and Prostaglandins to vasodilate the afferent arterioles and increase renin release.
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Initially, there is constriction of the efferent arterioles and dilation of afferent arterioles, with resulting glomerular capillary hypertension and hyperfiltration; this gradually changes to hypofiltration over time. Concurrently, there are changes within the glomerulus itself: these include a thickening of the basement membrane, a widening of the slit membranes of the podocytes, an increase in the number of mesangial cells, and an increase in mesangial matrix. This matrix invades the glomerular capillaries and produces deposits called Kimmelstiel-Wilson nodules. The mesangial cells and matrix can progressively expand and consume the entire glomerulus, shutting off filtration.
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Diagram of a capillary Blood flows from the heart through arteries, which branch and narrow into arterioles, and then branch further into capillaries where nutrients and wastes are exchanged. The capillaries then join and widen to become venules, which in turn widen and converge to become veins, which then return blood back to the heart through the venae cavae. In the mesentery, metarterioles form an additional stage between arterioles and capillaries. Individual capillaries are part of the capillary bed, an interweaving network of capillaries supplying tissues and organs.
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The more metabolically active a tissue is, the more capillaries are required to supply nutrients and carry away products of metabolism. There are two types of capillaries: true capillaries, which branch from arterioles and provide exchange between tissue and the capillary blood, and sinusoids, a type of open-pore capillary found in the liver, bone marrow, anterior pituitary gland, and brain circumventricular organs. Capillaries and sinusoids are short vessels that directly connect the arterioles and venules at opposite ends of the beds. Metarterioles are found primarily in the mesenteric microcirculation.
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The efferent arterioles of the undifferentiated cortical glomeruli are the most complex. Promptly on leaving the glomerulus they break up into capillaries and become part of a rich plexus of vessels surrounding the cortical portions of the renal tubules.
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Cardiac output is determined by stroke volume and heart rate; stroke volume is related to myocardial contractility and to the size of the vascular compartment. Peripheral resistance is determined by functional and anatomic changes in small arteries and arterioles.
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Pathology is due to both the adults and the eggs. Adults in the ileo-caecal arterioles cause an inflammatory (eosinophilic) response in humans. In the Cotton Rat the adult worms cause local haemorrhages. The intestinal wall is also affected.
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The slow blood flow in the straight arterioles makes them a likely location of thrombosis from thrombophilia, or tissue loss due to red blood cell sickling in sickle cell disease. Ischemia that results may lead to renal papillary necrosis.
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Acral arteriolar ectasia is characterized by purple serpiginous ectatic arterioles on the back of the fingers, presenting in the fifth decade of life.James, William; Berger, Timothy; Elston, Dirk (2005). Andrews' Diseases of the Skin: Clinical Dermatology. (10th ed.). Saunders.
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This hormone enhances the tachycardia and causes severe vasoconstriction of the arterioles to all but the essential organ in the body (especially the heart, lungs, and brain). These reactions usually correct the low arterial blood pressure (hypotension) very effectively.
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Additionally, this increase in temperature leads to an increase in basal metabolic temperature. The fish is now able to split ATP at a higher rate and ultimately can swim faster. The opah utilizes retia mirabilia to conserve heat, making it the newest addition to the list of regionally endothermic fish. Blood traveling through capillaries in the gills must carry cold blood due to their exposure to cold water, but retia mirabilia in the opah's gills are able to transfer heat from warm blood in arterioles coming from the heart that heats this colder blood in arterioles leaving the gills.
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At the point where the afferent arterioles enter the glomerulus and the efferent arteriole leaves it, the tubule of the nephron touches the arterioles of the glomerulus from which it arose. At this location, in the wall of the distal convoluted tubule, there is a modified region of tubular epithelium called the macula densa. Cells in the macula densa respond to changes in the sodium chloride levels in the distal tubule of the nephron via the tubuloglomerular feedback (TGF) loop. The macula densa's detection of elevated sodium chloride, which leads to an increase in GFR, is based on the concept of purinergic signaling.
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Counter current multiplier diagram The loop of Henle is supplied by blood in a series of straight capillaries descending from the cortical efferent arterioles. These capillaries (called the vasa recta; recta is from the Latin for "straight") also have a countercurrent multiplier mechanism that prevents washout of solutes from the medulla, thereby maintaining the medullary concentration. As water is osmotically driven from the descending limb into the interstitium, it readily enters the capillaries. The low bloodflow through the vasa recta allows time for osmotic equilibration, and can be altered by changing the resistance of the vessels' efferent arterioles.
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Furthermore, JG cells contain beta-1 adrenergic receptors, and so activation of the sympathetic nervous system will further stimulate renin release. Thus, a drop in blood pressure results in preferential vasodilation of the afferent arterioles, increasing renal blood flow (RBF), renal plasma flow (RPF) and GFR due to greater blood flow to the glomerulus. Note that there is no change in filtration fraction, as both GFR and RPF are increased. It also results in the release of renin, which, through the renin–angiotensin system, causes constriction of the efferent arterioles, which ultimately increases hydrostatic pressure in the glomerulus.
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The process triggered by the macula densa helps keep the GFR fairly steady in response to varying artery pressure. Damage to the macula densa would impact blood flow to the kidneys because the afferent arterioles would not dilate in response to a decrease in filtrate osmolarity and pressure at the glomerulus would not be increased. As part of the body's blood pressure regulation, the macula densa monitors filtrate osmolarity; if it falls too far, the macula densa causes the afferent arterioles of the kidney to dilate, thus increasing the pressure at the glomerulus and increasing the glomerular filtration rate.
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This acts on the kidneys to inhibit the secretion of renin and aldosterone causing the release of sodium, and accompanying water into the urine, thereby reducing the blood volume. This information is then conveyed, via afferent nerve fibers, to the solitary nucleus in the medulla oblongata. From here motor nerves belonging to the autonomic nervous system are stimulated to influence the activity of chiefly the heart and the smallest diameter arteries, called arterioles. The arterioles are the main resistance vessels in the arterial tree, and small changes in diameter cause large changes in the resistance to flow through them.
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Systemic vasculitides are a group of heterogeneous diseases that share the etiology in terms of inflammation of the blood vessels (vasculitis) – more specifically the arterioles – with systemic envolvement. Some examples of this group include granulomatosis with polyangiitis, polyarteritis nodosa, Behçet's disease, and HSP.
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Extraglomerular mesangial cells are located in the junction between the afferent and efferent arterioles. These cells have a contractile property similar to vascular smooth muscles and thus play a role in “regulating GFR” by altering the vessel diameter. Renin is also found in these cells.
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Br J Dermatol. 2003 Feb;148(2):342-5. The pathophysiology is still unclear, with most cases occurring sporadically, although rare cases were reported in families. Studies indicated the primary involvement of capillaries, venules and veins, and possibly also that of arterioles and lymphatics.
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There exist two cases: acute cerebral edema and acute pulmonary edema. The first one is caused by the vasodilatation of the cerebral blood vessels produced by the hypoxia; the second one is caused by the vasoconstriction of the pulmonary arterioles, caused by the hypoxia.
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Changes in retinal blood circulation are seen with aging and exposure to air pollution, and may indicate cardiovascular diseases such as hypertension and atherosclerosis. Determining the equivalent width of arterioles and venules near the optic disc is also a widely used technique to identify cardiovascular risks.
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The aorta is the root systemic artery (i.e., main artery). In humans, it receives blood directly from the left ventricle of the heart via the aortic valve. As the aorta branches and these arteries branch, in turn, they become successively smaller in diameter, down to the arterioles.
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As a consequence, microcirculation blood flow remains constant despite changes in systemic blood pressure. This mechanism is present in all tissues and organs of the human body. In addition, the nervous system participates in the regulation of microcirculation. The sympathetic nervous system activates the smaller arterioles, including terminals.
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In patients with ischemic heart disease there is an accumulation of angiogenic growth factors in the pericardial fluid. These contribute to angiogenesis (the formation of new blood vessels) and arteriogenesis (the increase in diameter of existing arterioles). This helps to prevent myocardial ischemia (lack of oxygen to the heart).
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Blanching of the skin often occurs when STS is injected into arterioles (small artery branches). Telangiectatic matting, or the development of tiny red vessels, is unpredictable and usually must be treated with repeat sclerotherapy or laser. Medscape. William R. Finkelmeier, What's New in ACS Surgery: Sclerotherapy. ACS Surgery 2003.
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The definitive diagnosis of HN requires morphological examination. Common histological features can be identified in the renal and glomerular vasculature. Glomerulosclerosis is often present, either focally or globally, which is characterized by hardening of the vessel walls. Also, luminal narrowing or the arteries and arterioles of the kidney system.
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The blood exiting the efferent arterioles of these nephrons enter the vasa recta, which are straight capillary branches that deliver blood to the renal medulla. These vasa recta run adjacent to the descending and ascending loop of Henle, and participate in the maintenance of the medullary countercurrent exchange system.
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Page 586. . A distinct vascular malformation, to our knowledge not described before, is reported. The malformation consists of purple serpiginous vessels on the dorsa of the digits, first arising in the fifth decade of life. The vessels are ectatic arterioles and are believed to represent a rare vascular malformation.
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The altered coat of the arterioles, consisting of adenoid tissue, presents here and there thickenings of a spheroidal shape, the white pulp. The arterioles end by opening freely into the splenic pulp; their walls become much attenuated, they lose their tubular character, and the endothelial cells become altered, presenting a branched appearance, and acquiring processes which are directly connected with the processes of the reticular cells of the pulp. In this manner the vessels end, and the blood flowing through them finds its way into the interstices of the reticulated tissue of the splenic pulp. Thus the blood passing through the spleen is brought into intimate relation with the elements of the pulp, and no doubt undergoes important changes.
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Molecular Interventions. 2003; 3: 79-89. Gap junctions are thought to play a large role in this synchronization, as application of gap junction blockers has been shown to abolish vasomotion, indicating a critical role.Haddock RE, Hirst GDS, Hill CE. Voltage independence of vasomotion in isolated irideal arterioles of the rat.
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27, p. 174 Encyclopædia Britannica, 1987 They are branching in a segmental distribution to the end arterioles and not anastomoses. This is clinically significant for diseases affecting choroidal blood supply. The macula responsible for central vision and the anterior part of the optic nerve are dependent on choroidal blood supply.
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The arterioles supply capillaries, which in turn empty into venules. The first branches off of the aorta are the coronary arteries, which supply blood to the heart muscle itself. These follow by the branches of the aortic arch, namely the brachiocephalic artery, the left common carotid, and the left subclavian arteries.
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Another theory suggests that individuals with Marfan syndrome have connective tissue dysplasia or vascular defects which in the case of tooth pulp, endothelial rupture of the pulp arterioles will lead to hemorrhagic areas in the pulp. It was proposed that these hemorrhagic areas in the pulp will induce mineralization within the pulp.
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In 1920, August Krogh was awarded the Nobel Prize in Physiology or Medicine for his discovering the mechanism of regulation of capillaries in skeletal muscle. Krogh was the first to describe the adaptation of blood perfusion in muscle and other organs according to demands through the opening and closing of arterioles and capillaries.
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Naphazoline is a medicine used as a decongestant. It is a sympathomimetic agent with marked alpha adrenergic activity. It is a vasoconstrictor with a rapid action in reducing swelling when applied to mucous membrane. It acts on alpha-receptors in the arterioles of the conjunctiva to produce constriction, resulting in decreased congestion.
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Werner syndrome patients are at increased risk for several other diseases, many associated with aging. Atherosclerosis, the thickening of artery walls due to cholesterol buildup, is one common complication. While normal atherosclerosis generally involves the major arteries, smaller arterioles are more likely to be affected. It is possible nervous system disorders are associated.
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Typically, vSMCs wrap around larger vessels: they form a dense continuum spindling around arteries, arterioles and precapillary arterioles; while around postcapillary venules, vSMCs adopt a different morphology: individual cell bodies extending thing branching processes, that become more stellate-like around venules and veins. The cell body of pericytes has a round shape extending a few processes in a longitudinal fashion along the capillaries. Recently, efforts have been undertaken using single cell sequencing on mural cells to try to characterize their molecular signature along the blood vessels. This showed that there is a zonation in their expression patterns by which they can be grouped into different subsets, but no singular markers have been found so far that can identify unequivocally any of the cell types.
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These ultimately leave the trabecular sheaths, and terminate in the proper substance of the spleen in small tufts or pencils of minute arterioles, which open into the interstices of the reticulum formed by the branched sustentacular cells. Each of the larger branches of the artery supplies chiefly that region of the organ in which the branch ramifies, having no anastomosis with the majority of the other branches. The arterioles, supported by the minute trabeculae, traverse the pulp in all directions in bundles (penicilli) of straight vessels. Their trabecular sheaths gradually undergo a transformation, become much thickened, and converted into adenoid tissue; the bundles of connective tissue becoming looser and their fibrils more delicate, and containing in their interstices an abundance of lymph corpuscles.
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It is a direct- acting smooth muscle relaxant and acts as a vasodilator primarily in resistance arterioles; the molecular mechanism involves inhibition of inositol trisphosphate-induced Ca2+ release from the sarcoplasmic reticulum in arterial smooth muscle cells. By relaxing vascular smooth muscle, vasodilators act to decrease peripheral resistance, thereby lowering blood pressure and decreasing afterload.
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The largest proportion of resistance in this series is contributed by the arterioles. Parallel resistance is illustrated by the circulatory system. Each organ is supplied by an artery that branches off the aorta. The total resistance of this parallel arrangement is expressed by the following equation: 1/Rtotal = 1/Ra \+ 1/Rb \+ ... 1/Rn.
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For cortical nephrons, a single network of capillaries, known as the peritubular capillaries, surrounds the entire renal tubule, whereas for juxtamedullary nephrons, the peritubular capillaries surround only the proximal and distal convoluted tubules, while another network branching from the efferent arteriole, known as the straight arterioles of kidney, surrounds the nephron loop (of Henle).
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Microangiopathy (or microvascular disease, or small vessel disease) is an angiopathy (i.e. disease of blood vessels) affecting small blood vessels in the body. It can be contrasted to macroangiopathy, or large vessel disease. Cerebral small vessel disease refers to a group of diseases that affect the small arteries, arterioles, venules, and capillaries of the brain.
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Noradrenaline and adrenaline have effects on alpha and beta adrenergic receptors. Other hormones (catecholamine, renin-angiotensin, vasopressin, and atrial natriuretic peptide) circulate in the bloodstream and can have an effect on the microcirculation causing vasodilation or vasoconstriction. Many hormones and neuropeptides are released together with classical neurotransmitters. Arterioles respond to metabolic stimuli that are generated in the tissues.
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Stimulation to orgasm is optimally achieved by a massaging sensation. Sexual arousal results in a number of physical changes in the vulva. During arousal vaginal lubrication increases. Vulva tissue is highly vascularised; arterioles dilate in response to sexual arousal and the smaller veins will compress after arousal, so that the clitoris and labia minora increase in size.
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The typical ANCAs in GPA are those that react with proteinase 3, an enzyme prevalent in neutrophil granulocytes. In vitro studies have found that ANCAs can activate neutrophils, increase their adherence to endothelium, and induce their degranulation that can damage endothelial cells. In theory, this phenomenon could cause extensive damage to the vessel wall, in particular of arterioles.
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Here, blood from the portal veins and the efferent arterioles are mixed and travel out of the kidneys through the efferent veins. Alternatively, blood can also flow towards the liver. Research indicates that kidneys of avian species receive approximately 10% to 15% of cardiac output. The renal blood of common ravens is composed of various molecules.
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A pulmonary artery is an artery in the pulmonary circulation that carries deoxygenated blood from the right side of the heart to the lungs. The largest pulmonary artery is the main pulmonary artery or pulmonary trunk from the heart, and the smallest ones are the arterioles, which lead to the capillaries that surround the pulmonary alveoli.
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This results in decreased resistance to blood flow through systemic arterioles, which decreases afterload (decreases the failing heart's workload) and reduces the amount of mitral regurgitation.Verdouw PD, Hartog JM, Duncker DJ, Roth W, Saxena PR. "Cardiovascular profile of pimobendan, a benzimidazole-pyridazinone derivative with vasodilating and inotropic properties." Eur J Pharmacol. 1986 Jul 15;126(1-2):21-30.
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The precise mechanism of acrocyanosis is not known. The current line of thinking goes that vasospasms in the cutaneous arteries and arterioles produce cyanotic discoloration, while compensatory dilatation in the postcapillary venules causes sweating. Arteriovenous subpapillary plexus shunting also occurs. Persistent vasoconstriction at the precapillary sphincter creates a local hypoxic environment, thus releasing adenosine into the capillary bed.
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When the arterial blood pressure rises the arterioles are stimulated to dilate making it easier for blood to leave the arteries, thus deflating them, and bringing the blood pressure down, back to normal. At the same time the heart is stimulated via cholinergic parasympathetic nerves to beat more slowly (called bradycardia), ensuring that the inflow of blood into the arteries is reduced, thus adding to the reduction in pressure, and correction of the original error. Low pressure in the arteries, causes the opposite reflex of constriction of the arterioles, and a speeding up of the heart rate (called tachycardia). If the drop in blood pressure is very rapid or excessive, the medulla oblongata stimulates the adrenal medulla, via "preganglionic" sympathetic nerves, to secrete epinephrine (adrenaline) into the blood.
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This is one contributor to high altitude sickness. On the other hand, if the switch to oxygen homeostasis is incomplete, then hypoxia may complicate the clinical picture with potentially fatal results. There are oxygen sensors in the smaller bronchi and bronchioles. In response to low partial pressures of oxygen in the inhaled air these sensors reflexively cause the pulmonary arterioles to constrict.
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These changes cause significant vasodilation. The reverse occurs when metabolic activity is slowed and these substances wash out of the tissues. The myogenic effect refers to the inherent attempt of vascular smooth muscle surrounding arterioles and arteries to maintain the tension in the wall of these blood vessels by dilating when internal pressure is reduced and to constrict when wall tension increases.
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Patients typically present with low frequency hearing loss detectable via an audiogram. Headaches are frequently present in addition to roaring tinnitus and often some degree of paranoia. Partial vision loss is often present and caused by branch retinal artery occlusions. The presence of refractile or non-refractile yellow Gass plaques in the retinal arterioles is near pathognomonic for the disease.
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AVMs are an abnormal connection between the arteries and veins in the human brain. Arteriovenous malformations are most commonly of prenatal origin. In a normal brain oxygen enriched blood from the heart travels in sequence through smaller blood vessels going from arteries, to arterioles and then capillaries. Oxygen is removed in the latter vessel to be used by the brain.
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Power Doppler is a Doppler sequence that measures the ultrasonic energy backscattered from red blood cells in each pixel of the image. It provides no information on blood velocity but is proportional to blood volume within the pixel. However, conventional power Doppler imaging lacks sensitivity to detect small arterioles/venules and thus is unable to provide local neurofunctional information through neurovascular coupling.
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Binding to ATP mediates synaptic transmission between neurons and from neurons to smooth muscle, being responsible, for example, for sympathetic vasoconstriction in small arteries, arterioles and vas deferens. Mouse studies suggest that this receptor is essential for normal male reproductive function. It is possible that the development of selective antagonists for this receptor may provide an effective non-hormonal male contraceptive pill.
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The last phase was the production of a wheal filled fluid over the original spot. Lewis believed that the skin’s response was due to the dilation of neighboring blood vessels that were triggered by the nervous system through the axon reflex. This triphasic response was named the triple response of Lewis. The dilation of arterioles in the effected area is due to vasodilation.
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Age-related and hypertension-related small vessel diseases and cerebral amyloid angiopathy are the most common forms. Coronary small vessel disease is a type of coronary heart disease (CHD) that affects the arterioles and capillaries of the heart. Coronary small vessel disease is also known as microvascular angina, microvascular dysfunction, non-obstructive coronary disease, or in the past, cardiac syndrome X.
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In the kidney, the macula densa is an area of closely packed specialized cells lining the wall of the distal tubule, at the point where the thick ascending limb of the Loop of Henle meets the distal convoluted tubule. The macula densa is the thickening where the distal tubule touches the glomerulus. The cells of the macula densa are sensitive to the concentration of sodium chloride in the distal convoluted tubule. A decrease in sodium chloride concentration initiates a signal from the macula densa that has two effects: (1) it decreases resistance to blood flow in the afferent arterioles, which raises glomerular hydrostatic pressure and helps return the glomerular filtration rate (GFR) toward normal, and (2) it increases renin release from the juxtaglomerular cells of the afferent and efferent arterioles, which are the major storage sites for renin.
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For the kidney structure, see straight arterioles of kidney Vasa recta are straight arteries coming off from arcades in the mesentery of the jejunum and ileum, and heading toward the intestines. The arcades are anastomoses of the jejunal and ileal arteries, branches of superior mesenteric artery. The vasa recta of the jejunum are long and few, compared to the ileum where they are numerous and short.
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Hematocrit levels also serve as an indicator of health conditions. Thus, tests on hematocrit levels are often carried out in the process of diagnosis of such conditions, and may be conducted prior to surgery. Additionally, the health conditions associated with certain hematocrit levels are the same as ones associated with certain hemoglobin levels.As blood flows from the arterioles into the capillaries, a change in pressure occurs.
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In order to maintain pressure, the capillaries branch off to a web of vessels that carry blood into the venules. Through this process blood undergoes micro-circulation. In micro- circulation, the Fåhræus effect will take place, resulting in a large change in hematocrit. As blood flows through the arterioles, red cells will act a feed hematocrit (Hf), while in the capillaries, a tube hematocrit (Ht) occurs.
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Epiploic appendages are also called appendices epiploicae. The appendages themselves are 50–100 appendages that are oriented in two rows anterior and posterior. The appendages are parallel to the superficial section of the taenia coli. Furthermore, the appendages are between 0.5 and 5 cm long, each appendage is attached with one or two arterioles and a venule within vascular stalks attached to the colon.
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Goldberg classified PSR into following 5 different self-explanatory stages: # Stage of peripheral arterial occlusion and ischemia: It is the earliest abnormality that can be visualized by fundus examination. The occluded arterioles can be seen as dark red lines. They eventually turn into white silver-wire vessels. # Stage of peripheral arteriolar-venular anastomoses: Arteriolar-venular anastomoses develop as blood is diverted from blocked arteries to nearby venules.
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Thrombotic microangiopathy (TMA) is a pathology that results in thrombosis in capillaries and arterioles, due to an endothelial injury. It may be seen in association with thrombocytopenia, anemia, purpura and kidney failure. The classic TMAs are hemolytic uremic syndrome and thrombotic thrombocytopenic purpura. Other conditions with TMA include atypical hemolytic uremic syndrome, disseminated intravascular coagulation, scleroderma renal crisis, malignant hypertension, antiphospholipid antibody syndrome, and drug toxicities, e.g.
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The pulmonary arteries are blood vessels that carry blood from the right side of the heart through to the capillaries of the lungs. The blood that is carried is, unlike other arteries, without oxygen ("deoxygenated"). The main pulmonary arteries emerge from the right side of the heart, and these split into smaller arteries that progressively divide and become smaller until they become arterioles and eventually capillaries.
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They may be composed of abnormal aggregations of arterioles, capillaries or venules. Because telangiectasias are vascular lesions, they blanch when tested with diascopy. Telangiectasias, aside from presenting in many other conditions, are one of the features of the acronymically named CREST syndrome, a form of systemic scleroderma. The syndrome recognises the significantly co-presenting symptoms of calcinosis, Raynaud's phenomenon, esophageal dysmotility, sclerodactyly and telangiectasia.
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Vasovagal collapse – most frequent systemic complication. Cause for vasovagal collapse is due to the activation of parasympathetic nervous system and inhibition of the parasympathetic nervous system. These lead to a reduction in heart frequency and dilation of arterioles in the muscle causing reduced blood circulation in the brain. If vasovagal collapse occurs, put patient in the supine position with the feet higher than the head.
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Raynaud's phenomenon is frequently the first manifestation of CREST/lcSSc, preceding other symptoms by years. Stress and cold temperature induce an exaggerated vasoconstriction of the small arteries, arterioles, and thermoregulatory vessels of the skin of the digits. Clinically this manifests as a white-blue-red transition in skin color. Underlying this transition is pallor and cyanosis of the digits, followed by a reactive hyperemia as they rewarm.
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The spleen is a center of activity of the mononuclear phagocyte system and can be considered analogous to a large lymph node, as its absence causes a predisposition to certain infections. Like the thymus, the spleen has only efferent lymphatic vessels. Both the short gastric arteries and the splenic artery supply it with blood. The germinal centers are supplied by arterioles called penicilliary radicles.
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The trabecular arteries are the name of the branches of the splenic artery after it passes into the trabeculae of the spleen, where it branches. When these arteries then reach the white pulp, and become covered with periarteriolar lymphoid sheaths, the name changes again to central arteries (or central arterioles). Branches of the central arteries are given to the red pulp, and these are called penicillar arteries).
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Histologically, the glomeruli show thickened and sometimes split capillary walls due largely to endothelial swelling. Large deposits of fibrin-related materials in the capillary lumens, subendothelially, and in the mesangium are also found along with mesangiolysis. Interlobular and afferent arterioles show fibrinoid necrosis and intimal hyperplasia and are often occluded by thrombi. STEC-HUS most often affects infants and young children, but also occurs in adults.
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Mephentermine appears to act by indirect stimulation of β-adrenergic receptors causing the release of norepinephrine from its storage sites. It has a positive inotropic effect on the myocardium. AV conduction and refractory period of AV node is shortened with an increase in ventricular conduction velocity. It dilates arteries and arterioles in the skeletal muscle and mesenteric vascular beds, leading to an increase in venous return.
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Small vessels like vasa vasorum and vasa nervorum are particularly susceptible to external mechanical compression. A decrease in blood flow through the vasa nervorum has been implicated in the development of diabetic neuropathy. Arteritis of the vasa nervorum leads to mononeuritis multiplex or polyneuropathy. Occlusion of vasa nervorum at the level of the epineurial arterioles leads to ischemia of nerves, leading to vasculitic neuropathy.
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An alternative mechanism of hypertensive nephropathy is prolonged glomerular hypertension and hence glomerular hyperfiltration. These can occur simultaneously but not necessarily. The idea is that hypertension results in sclerosis of the glomeruli which ultimately means reduced kidney function. As a compensatory mechanism, the unaffected nephrons (specifically, the preglomerular arterioles) vasodilate to increase blood flow to the kidney perfusion and increase glomerular filtration across undamaged glomeruli.
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Prorenin () is a protein that constitutes a precursor for renin, the hormone that activates the renin–angiotensin system, which serves to raise blood pressure. Prorenin is converted into renin by the juxtaglomerular cells, which are specialised smooth muscle cells present mainly in the afferent, but also the efferent, arterioles of the glomerular capillary bed. Prorenin is a relatively large molecule, weighing approximately 46 KDa.
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Diagram showing the basic outline of nephron structure and function: diabetic nephropathy is associated with changes in the afferent and efferent arterioles, causing capillary hypertension; and damage to the glomerular capillaries of multiple causes, including mesangial matrix deposition The disease progression of diabetic nephropathy involves various clinical stages: hyperfiltration, microalbuminuria, macroalbuminuria, nephrotic proteinuria to progressive chronic kidney disease leading to end- stage renal disease (ESRD). The damage is exerted on all compartments of the kidney: the glomerulus, the renal tubules, the vasculature (afferent and efferent renal arterioles) and the interstitium. Renal fibrosis is the final common pathway of DN. This fibrosis is a product of multiple mechanisms including renal hemodynamic changes, glucose metabolism abnormalities associated with oxidative stress as well as inflammatory processes and an overactive renin-angiotensin-aldosterone system (RAAS). The pathophysiology of diabetic nephropathy is thought to involve an interaction between hemodynamic and metabolic factors.
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The retinal circulation undergoes a series of pathophysiological changes in response to elevated blood pressure. In the initial, vasoconstrictive stage, there is vasospasm and an increase in retinal arteriolar tone owing to local autoregulatory mechanisms. This stage is seen clinically as a generalized narrowing of the retinal arterioles. Persistently elevated blood pressure leads to intimal thickening, hyperplasia of the media wall, and hyaline degeneration in the subsequent, sclerotic, stage.
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Series circuits for train lighting were superseded, first by motor-generators, then by solid state devices. Series resistance can also be applied to the arrangement of blood vessels within a given organ. Each organ is supplied by a large artery, smaller arteries, arterioles, capillaries, and veins arranged in series. The total resistance is the sum of the individual resistances, as expressed by the following equation: Rtotal = Rartery \+ Rarterioles \+ Rcapillaries.
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A metarteriole is a short microvessel in the microcirculation that links arterioles and capillaries. Instead of a continuous tunica media, they have individual smooth muscle cells placed a short distance apart, each forming a precapillary sphincter that encircles the entrance to that capillary bed. Constriction of these sphincters reduces or shuts off blood flow through their respective capillary beds. This allows the blood to be diverted to elsewhere in the body.
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Rheumatic fever is a systemic disease affecting the connective tissue around arterioles, and can occur after an untreated strep throat infection, specifically due to group A streptococcus (GAS), Streptococcus pyogenes. It is believed to be caused by antibody cross- reactivity. This cross-reactivity is a type II hypersensitivity reaction and is termed molecular mimicry. Usually, self reactive B cells remain anergic in the periphery without T cell co-stimulation.
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The kidneys appear symmetrically atrophic and there is a reduced nephron mass. The kidneys have a surface of diffuse, fine granularity that resembles grain leather. Microscopically, the basic anatomic change consists of hyaline thickening of the walls of the small arteries and arterioles (hyaline arteriolosclerosis). Under a microscope, this appears as a homogeneous, pink hyaline thickening at the expense of the vessel lumina, with loss of underlying cellular detail.
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In all veins apart from the pulmonary vein, the saturation of hemoglobin is about 75%. (The values are reversed in the pulmonary circulation.) In addition to carrying oxygen, blood also carries hormones, waste products and nutrients for cells of the body. Blood vessels do not actively engage in the transport of blood (they have no appreciable peristalsis). Blood is propelled through arteries and arterioles through pressure generated by the heartbeat.
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Vasoconstriction is the narrowing of the blood vessels resulting from contraction of the muscular wall of the vessels, in particular the large arteries and small arterioles. The process is the opposite of vasodilation, the widening of blood vessels. The process is particularly important in controlling hemorrhage and reducing acute blood loss. When blood vessels constrict, the flow of blood is restricted or decreased, thus retaining body heat or increasing vascular resistance.
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In the absence of hydrostatic effects (e.g. standing), mean blood pressure decreases as the circulating blood moves away from the heart through arteries and capillaries due to viscous losses of energy. Mean blood pressure drops over the whole circulation, although most of the fall occurs along the small arteries and arterioles. Pulsatility also diminishes in the smaller elements of the arterial circulation, although some transmitted pulsatility is observed in capillaries.
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This Windkessel effect of the great elastic arteries has important biomechanical implications. The elastic recoil helps conserve the energy from the pumping heart and smooth out the pulsatile nature created by the heart. Aortic pressure is highest at the aorta and becomes less pulsatile and lower pressure as blood vessels divide into arteries, arterioles, and capillaries such that flow is slow and smooth for gases and nutrient exchange.
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Guyton & Hall Textbook Of Physiology, 11th Edition 2006, p. 324 As such, an increase in sodium chloride concentration would result in vasoconstriction of afferent arterioles, and reduced paracrine stimulation of juxtaglomerular cells. This demonstrates the macula densa feedback, where compensatory mechanisms act in order to return GFR to normal. The release of renin is an essential component of the renin–angiotensin–aldosterone system (RAAS), which regulates blood pressure and volume.
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Buschke-Ollendorff syndrome, Menkes disease, pseudoxanthoma elasticum, and Marfan's syndrome have been associated with defects in copper metabolism and lysyl oxidase or defects in the microfibril (defects in fibrillin, or fibullin for example). Hurler disease, a lysosomal storage disease, is associated with an altered elastic matrix. Hypertension and some congenital heart defects are associated with alterations in the great arteries, arteries, and arterioles with alterations in the elastic matrix.
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The pulmonary and the systemic circulations are the two parts of the vasculature. The pulmonary circulation system consists of the network of blood vessels from the right heart to the lungs and back to the left heart. The rest of the blood flow loop is called systemic circulation system. The pulmonary and systemic circulations take the blood through large arteries first and then branches into smaller arteries before reaching arterioles and capillaries.
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Diseases associated with cerebral atherosclerosis include: ;Hypertensive arteriopathy This pathological process involves the thickening and damage of arteriole walls. It mainly affects the ends of the arterioles which are located in the deep gray nuclei and deep white matter of the brain. It is thought that this is what causes cerebral microbleeds in deep brain regions. This small vessel damage can also reduce the clearance of amyloid-β, thereby increasing the likelihood of CAA.
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As a result of its breakdown to nitric oxide (NO), sodium nitroprusside has potent vasodilating effects on arterioles and venules (veins more than arteries) but this selectivity is much less marked than that of nitroglycerin. Sodium nitroprusside breaks down in circulation to release nitric oxide (NO). It does this by binding to oxyhaemoglobin to release cyanide, methaemoglobin and nitric oxide. NO activates guanylate cyclase in vascular smooth muscle and increases intracellular production of cGMP.
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This induces gas and nutrients to move from the blood to the cells, due to the lower osmotic pressure outside the capillary. The opposite process occurs when the blood leaves the capillaries and enters the venules, where the blood pressure drops due to an increase in flow rate. Arterioles receive autonomic nervous system innervation and respond to various circulating hormones in order to regulate their diameter. Retinal vessels lack a functional sympathetic innervation.
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Lymphatic capillaries are slightly larger in diameter than blood capillaries, and have closed ends (unlike the blood capillaries open at one end to the arterioles and open at the other end to the venules). This structure permits interstitial fluid to flow into them but not out. Lymph capillaries have a greater internal oncotic pressure than blood capillaries, due to the greater concentration of plasma proteins in the lymph.Guyton, Arthur; Hall, John (2006).
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Each arcuate artery supplies several interlobular arteries that feed into the afferent arterioles that supply the glomeruli. After filtration occurs, the blood moves through a small network of venules that converge into interlobular veins. As with the arteriole distribution, the veins follow the same pattern: the interlobular provide blood to the arcuate veins then back to the interlobar veins, which come to form the renal vein exiting the kidney for transfusion for blood.
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Measuring the pulse wave velocity (invasively and non-invasively) is a means of determining arterial stiffness. Maximum aortic velocity may be noted as Vmax or less commonly as AoVmax. Mean arterial pressure (MAP) is highest in the aorta, and the MAP decreases across the circulation from aorta to arteries to arterioles to capillaries to veins back to atrium. The difference between aortic and right atrial pressure accounts for blood flow in the circulation.
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This drainage prevents loss of water by both lowering volume and increasing concentration of the urine. Angiotensin, on the other hand, causes vasoconstriction on the systemic arterioles, and acts as a dipsogen for ostriches. Both of these antidiuretic hormones work together to maintain water levels in the body that would normally be lost due to the osmotic stress of the arid environment. The end-product of catabolism of protein metabolism in animals is nitrogen.
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19-HETE is an inhibitor of 20-HETE, a broadly active signaling molecule, e.g. it constricts arterioles, elevates blood pressure, promotes inflammation responses, and stimulates the growth of various types of tumor cells; however the in vivo ability and significance of 19-HETE in inhibiting 20-HETE has not been demonstrated (see 20-Hydroxyeicosatetraenoic acid). The EDP (see Epoxydocosapentaenoic acid) and EEQ (see epoxyeicosatetraenoic acid) metabolites have a broad range of activities.
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This causes diminished blood flow in tissues, so oxygen distribution decreases. The vasoconstriction of the pulmonary arterioles is caused by hypoxia in the right portion of the heart. Arteriole spasms include the major part of the blood flow through the pulmonary vessels, producing a short circuit in the blood flow giving less oxygen in blood. The person will recover if there is an administration of oxygen or if s/he is taken to low altitudes.
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These cells have characteristic positions, with alpha cells (secreting glucagon) tending to be situated around the periphery of the islet, and beta cells (secreting insulin) more numerous and found throughout the islet. Enterochromaffin cells are also scattered throughout the islets. Islets are composed of up to 3,000 secretory cells, and contain several small arterioles to receive blood, and venules that allow the hormones secreted by the cells to enter the systemic circulation.
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Flushing - a short-term dilatation of skin arterioles, causing reddish skin color - usually lasts for about 15 to 30 minutes, although sometimes can persist for weeks. Typically, the face is affected, but the reaction can extend to neck and upper chest. The cause is blood vessel dilation due to elevation in prostaglandin GD2 (PGD2) and serotonin. Flushing was often thought to involve histamine, but histamine has been shown not to be involved in the reaction.
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In mammals, an elegant rete mirabile in the efferent arterioles of juxtamedullary glomeruli is important in maintaining the hypertonicity of the renal medulla. It is the hypertonicity of this zone, resorbing water osmotically from the renal collecting ducts as they exit the kidney, that makes possible the excretion of a hypertonic urine and maximum conservation of body water. Vascular retia mirabilia are also found in the limbs of a range of mammals. These reduce the temperature in the extremities.
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Also arterial hyalinosis and arteriolar hyalinosis refers to thickening of the walls of arterioles by the deposits that appear as homogeneous pink hyaline material in routine staining. It is a type of arteriolosclerosis, which refers to thickening of the arteriolar wall and is part of the ageing process. ;Associations It is associated with aging, hypertension, diabetes mellitus and may be seen in response to certain drugs (calcineurin inhibitors). It is often seen in the context of kidney pathology.
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3D Medical animation still showing Normal blood vessel (L) Vs. Vasodilation (R) Vasodilation is the widening of blood vessels. It results from relaxation of smooth muscle cells within the vessel walls, in particular in the large veins, large arteries, and smaller arterioles. The process is the opposite of vasoconstriction, which is the narrowing of blood vessels. When blood vessels dilate, the flow of blood is increased due to a decrease in vascular resistance and increase in cardiac output.
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Therefore, dilation of arterial blood vessels (mainly the arterioles) decreases blood pressure. The response may be intrinsic (due to local processes in the surrounding tissue) or extrinsic (due to hormones or the nervous system). In addition, the response may be localized to a specific organ (depending on the metabolic needs of a particular tissue, as during strenuous exercise), or it may be systemic (seen throughout the entire systemic circulation). Endogenous substances and drugs that cause vasodilation are termed vasodilators.
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Although it is recognized that the sympathetic nervous system plays an expendable role in vasodilation, it is only one of the mechanisms by which vasodilation can be accomplished. The spinal cord has both vasodilation and vasoconstriction nerves. The neurons that control vascular vasodilation originate in the hypothalamus. Some sympathetic stimulation of arterioles in skeletal muscle is mediated by epinephrine acting on β-adrenergic receptors of arteriolar smooth muscle, which would be mediated by cAMP pathways, as discussed above.
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In a healthy vascular system the endothelium lines all blood-contacting surfaces, including arteries, arterioles, veins, venules, capillaries, and heart chambers. This healthy condition is promoted by the ample production of nitric oxide by the endothelium, which requires a biochemical reaction regulated by a complex balance of polyphenols, various nitric oxide synthase enzymes and L-arginine. In addition there is direct electrical and chemical communication via gap junctions between the endothelial cells and the vascular smooth muscle.
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Further local responses to stretch, carbon dioxide, pH, and oxygen also influence arteriolar tone. Generally, norepinephrine and epinephrine (hormones produced by sympathetic nerves and the adrenal gland medulla) are vasoconstrictive acting on alpha 1-adrenergic receptors. However, the arterioles of skeletal muscle, cardiac muscle, and pulmonary circulation vasodilate in response to these hormones when they act on beta-adrenergic receptors. Generally, stretch and high oxygen tension increase tone, and carbon dioxide and low pH promote vasodilation.
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Most symptoms of peanut allergy are related to the action of immunoglobulin E (IgE) and other anaphylatoxins which act to release histamine and other mediator substances from mast cells (degranulation). In addition to other effects, histamine induces vasodilation of arterioles and constriction of bronchioles in the lungs, also known as bronchospasm. Symptoms can also include mild itchiness, hives, angioedema, facial swelling, rhinitis, vomiting, diarrhea, acute abdominal pain, exacerbation of atopic eczema, asthma, and cardiac arrest. Anaphylaxis may occur.
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Isoprenaline is a β1 and β2 adrenoreceptor agonist and has almost no activity on alpha adrenergic receptors. Its agonist effects at TAAR1 provide it with a pharmacodynamic effects that resemble those of the endogenous trace amines, like tyramine. "Table 1: EC50 values of different agonists at hTAAR1, hADRB1 and hADRB2." Isoprenaline's effects on the cardiovascular system (non-selective) relate to its actions on cardiac β1 receptors and β2 receptors on smooth muscle within the tunica media of arterioles.
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The following terms are similar, yet distinct, in both spelling and meaning, and can be easily confused: arteriosclerosis, arteriolosclerosis, and atherosclerosis. Arteriosclerosis is a general term describing any hardening (and loss of elasticity) of medium or large arteries (); arteriolosclerosis is any hardening (and loss of elasticity) of arterioles (small arteries); atherosclerosis is a hardening of an artery specifically due to an atheromatous plaque (). The term atherogenic is used for substances or processes that cause formation of atheroma.
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Blood vessels function to transport blood. In general, arteries and arterioles transport oxygenated blood from the lungs to the body and its organs, and veins and venules transport deoxygenated blood from the body to the lungs. Blood vessels also circulate blood throughout the circulatory system Oxygen (bound to hemoglobin in red blood cells) is the most critical nutrient carried by the blood. In all arteries apart from the pulmonary artery, hemoglobin is highly saturated (95–100%) with oxygen.
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Cryosurgery may cause complications due to damage of underlying structures. Destruction of the basement membrane may cause scarring and destruction of hair follicles can cause alopecia or hair loss. Occasionally, hypopigmentation may occur in the area of skin treated with cryosurgery, however, this complication is usually transient and often resolves as melanocytes migrate and repigment the area over several months. Bleeding can also occur, which can be delayed or immediate, due to damage of underlying arteries and arterioles.
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It generally occurs in small arteries or arterioles and is commonly due to hypertension, intracranial vascular malformations (including cavernous angiomas or arteriovenous malformations), cerebral amyloid angiopathy, or infarcts into which secondary hemorrhage has occurred. Other potential causes are trauma, bleeding disorders, amyloid angiopathy, illicit drug use (e.g., amphetamines or cocaine). The hematoma enlarges until pressure from surrounding tissue limits its growth, or until it decompresses by emptying into the ventricular system, CSF or the pial surface.
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In the left heart, oxygenated blood is returned to the left atrium via the pulmonary veins. It is then pumped into the left ventricle through the mitral valve and into the aorta through the aortic valve for systemic circulation. The aorta is a large artery that branches into many smaller arteries, arterioles, and ultimately capillaries. In the capillaries, oxygen and nutrients from blood are supplied to body cells for metabolism, and exchanged for carbon dioxide and waste products.
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A resistance artery is small diameter blood vessel in the microcirculation that contributes significantly to the creation of the resistance to flow and regulation of blood flow. Resistance arteries are usually arterioles or end- points of arteries. Having thick muscular walls and narrow lumen they contribute the most to the resistance to blood flow. Degree of the contraction of muscles in the wall of a resistance artery is directly connected to the size of the lumen.
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The Heart, arteries, and veins (a network of tubes to carry blood) constitute the cardiovascular system or circulatory system of our body which transports the blood throughout the body. The heart can be thought of as a muscular pump, consisting of four chambers, and pulsatile muscles which pump and circulates the blood through the vasculature. Arteries, arterioles, capillaries, venules, and veins make up the vasculature. The cardiovascular system circulates about 5 liters of blood at a rate of approximately 6 l/m.
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Each arcuate artery supplies several interlobular arteries that feed into the afferent arterioles that supply the glomeruli. Blood drains from the kidneys, ultimately into the inferior vena cava. After filtration occurs, the blood moves through a small network of small veins (venules) that converge into interlobular veins. As with the arteriole distribution, the veins follow the same pattern: the interlobular provide blood to the arcuate veins then back to the interlobar veins, which come to form the renal veins which exiting the kidney .
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The Windkessel analogy illustrated. Windkessel effect is a term used in medicine to account for the shape of the arterial blood pressure waveform in terms of the interaction between the stroke volume and the compliance of the aorta and large elastic arteries (Windkessel vessels) and the resistance of the smaller arteries and arterioles. Windkessel when loosely translated from German to English means 'air chamber', but is generally taken to imply an elastic reservoir. The walls of large elastic arteries (e.g.
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When demand for oxygen in the myocardium is increased, the vascular resistance of the coronary arteries has the ability to reduce, and this can increase the volume of blood passing through the blood vessels. This reduction occurs because the arteries dilate, which causes an increase in the diameter of the lumen. The greatest potential for this change is normally in the branches (arterioles) of the coronary artery that penetrate the myocardium, rather than those on the surface of the heart.
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Decreased cardiac output despite normal blood volume, due to severe congestive heart failure, large myocardial infarction, heart valve problems, or extremely low heart rate (bradycardia), often produces hypotension and can rapidly progress to cardiogenic shock. Arrhythmias often result in hypotension by this mechanism. Excessive vasodilation, or insufficient constriction of the blood vessels (mostly arterioles), causes hypotension. This can be due to decreased sympathetic nervous system output or to increased parasympathetic activity occurring as a consequence of injury to the brain or spinal cord.
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A capillary is a small blood vessel from 5 to 10 micrometres (μm) in diameter, and having a wall one endothelial cell thick. They are the smallest blood vessels in the body: they convey blood between the arterioles and venules. These microvessels are the site of exchange of many substances with the interstitial fluid surrounding them. Substances which exit include water (proximal portion), oxygen, and glucose; substances which enter include water (distal portion), carbon dioxide, uric acid, lactic acid, urea and creatinine.
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Merozoites emerge from the second-generation meronts and enter the mononucleated cells, where they develop by endodyogeny. Subsequent generations of merozoites develop downstream in the direction of blood flow to arterioles, capillaries, venules, and veins throughout the body, subsequently developing into the final asexual generation in muscles. Merozoites entering muscle cells round up to form metrocytes and initiate sarcocyst formation. Sarcocysts begin as unicellular bodies containing a single metrocyte and through asexual multiplication numerous metrocytes accumulate and the sarcocyst increases in size.
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This leads to sympathetic nerve activation, resulting in renin secretion through β 1 -receptors. Constriction of the afferent arterioles causes a decrease in the intraglomerular pressure, reducing GFR proportionally. Renin is the main effector of the juxtaglomerular baroreceptors. Renin is secreted from granules in the JG cells, and once in the blood stream, it acts as a protease to convert angiotensinogen to angiotensin I, which is converted by angiotensin converting enzyme, to angiotensin II, which, in turn, stimulates aldosterone release.
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Because adenosine acts as a direct vasodilator, it is not dependent on an intact endothelium to cause vasodilation. Adenosine causes vasodilation in the small and medium-sized resistance arterioles (less than 100 µm in diameter). When adenosine is administered it can cause a coronary steal phenomenon, where the vessels in healthy tissue dilate as much as the ischemic tissue and more blood is shunted away from the ischemic tissue that needs it most. This is the principle behind adenosine stress testing.
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Weber continued his research on blood and in 1827, he made another significant finding. Weber explained the elasticity of blood vessels in the movement of blood in the aorta in a continuous flow to the capillaries and arterioles. Two-point Threshold Technique: helped map sensitivity and touch acuity on the body using compass technique. Points of a compass would be set at varying distances in order to see at what distance are the points of the compass perceived as two separate points instead of one single point.
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Capillary shunting is blood that passes through capillaries of unventilated alveoli or deoxygenated blood flowing directly from pulmonary arterioles to nearby pulmonary veins through anastomoses, bypassing the alveolar capillaries. In addition, some of the smallest cardiac veins drain directly into the left ventricle of the human heart. This drainage of deoxygenated blood straight into the systemic circulation is why the arterial PO2 is normally slightly lower than the alveolar PO2, known as the alveolar–arterial gradient, a useful clinical sign in determining the cause of hypoxia.
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Women with myocardial ischemia often have either no or atypical symptoms, such as palpitations, anxiety, weakness, and fatigue. Additionally, many women with angina are found to have cardiac ischemia, yet no evidence of obstructive coronary artery disease on cardiac catheterization. Evidence is accumulating that nearly half of women with myocardial ischemia suffer from coronary microvascular disease, a condition often called microvascular angina (MVA). Small intramyocardial arterioles constrict in MVA causing ischemic pain that is less predictable than with typical epicardial coronary artery disease (CAD).
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For over 100 years vasospasms are known, particularly in the vessels supplying the retina of the eye with blood. These vasospasms are temporary narrowings of arteries or arterioles, which result in an insufficient supply of blood of the corresponding organs or parts of organs. Such spasms can occur at various locations in the human body; in this case medical terminology calls it "vasospastic syndrome". Over the years, it has been established that these spasms are usually part of a general dysregulation of blood vessels.
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The extraglomerular mesangial cells are found between the afferent and efferent arterioles towards the vascular pole of the glomerulus. The extraglomerular mesangial cells are adjacent to the intraglomerular mesangial cells that are located inside the glomerulus and in between the capillaries. The primary function of mesangial cells is to remove trapped residues and aggregated protein from the basement membrane thus keeping the filter free of debris. The contractile properties of mesangial cells have been shown to be insignificant in changing the filtration pressure of the glomerulus.
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Cortical radial arteries, formerly known as interlobular arteries, are renal blood vessels given off at right angles from the side of the arcuate arteries looking toward the cortical substance. The interlobular arteries pass directly outward between the medullary rays to reach the fibrous tunic, where they end in the capillary network of this part. These vessels do not anastomose with each other, but form end-arteries. In their outward course, they give off lateral branches, which are the afferent arterioles that supply the renal corpuscles.
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Venule walls have three layers: An inner endothelium composed of squamous endothelial cells that act as a membrane, a middle layer of muscle and elastic tissue and an outer layer of fibrous connective tissue. The middle layer is poorly developed so that venules have thinner walls than arterioles. They are porous so that fluid and blood cells can move easily from the bloodstream through their walls. Short portal venules between the neural and anterior pituitary lobes provide an avenue for rapid hormonal exchange via the blood.
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Myocardium itself is well vascularized, with highly branched arterioles and venules, as well as a high degree of capillarization. Major arteries and veins run longitudinally to and from the red swimming muscles, which are found close to the spinal column, just underneath the skin. Small arteries branch off and penetrate the red muscle, delivering oxygenated blood, whereas veins take deoxygenated blood back to the heart. The red muscles also have a high myoglobin content and capillary density, where many of the capillaries branch off.
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The discovery of the axonal reflex found that the axon reflex activates local arterioles causing vasodilation and muscle contraction. This muscle contraction was observed in people with asthma where the released neuropeptides caused the smooth muscle in the airway to contract. Similarly the release of cholinergic agents at sudomotor nerve terminals evokes an axon reflex that stimulates sweat glands inducing the body to sweat in response to heat. The axon reflex is possible through the transmission of signals from the cutaneous receptors on the skin.
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If the kidney is methodologically perfused at moderate pressures (90–220 mm Hg performed on an experimental animal; in this case, a dog), then, there is a proportionate increase of: -Renal Vascular Resistance Along with the increase in pressure. At low perfusion pressures, Angiotensin II may act by constricting the efferent arterioles, thus mainlining the GFR and playing a role in autoregulation of Renal Blood Flow. People with poor blood flow to the kidneys caused by medications that inhibit angiotensin-converting enzyme may face kidney failure.
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Three common macrovascular diseases are coronary disease (in the heart), cerebrovascular disease (in the brain), and peripheral vascular disease (in the limbs) Macrovascular disease (macroangiopathy) refers to atherosclerosis. Atherosclerosis is a form of arteriosclerosis (thickening and hardening of arterial walls), characterized by plaque deposits of lipids, fibrous connective tissue, calcium, and other blood substances. Atherosclerosis, by definition, affects only medium and large arteries (excluding arterioles). Macrovascular disease is associated with the development of coronary artery disease, peripheral vascular disease, brain attack (stroke), and increased risk of infection.
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Hypertension is a risk factor for chronic kidney disease and end-stage kidney disease (ESKD). Kidney risk appears to be more closely related to systolic than to diastolic blood pressure, and black men are at greater risk than white men for developing ESRD at every level of blood pressure. The atherosclerotic, hypertension-related vascular lesions in the kidney primarily affect the preglomerular arterioles, resulting in ischemic changes in the glomeruli and postglomerular structures. Glomerular injury may also be a consequence of direct damage to the glomerular capillaries due to glomerular hyperperfusion.
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Glomerular pathology progresses to glomerulosclerosis, and eventually the kidney tubules may also become ischemic and gradually atrophic. The kidney lesion associated with malignant hypertension consists of fibrinoid necrosis of the afferent arterioles, sometimes extending into the glomerulus, and may result in focal necrosis of the glomerular tuft. Clinically, macroalbuminuria (a random urine albumin/creatinine ratio > 300 mg/g) or microalbuminuria (a random urine albumin/creatinine ratio 30–300 mg/g) are early markers of kidney injury. These are also risk factors for kidney disease progression and for cardiovascular disease.
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Most vessels of the microcirculation are lined by flattened cells of the endothelium and many of them are surrounded by contractile cells called pericytes. The endothelium provides a smooth surface for the flow of blood and regulates the movement of water and dissolved materials in the interstitial plasma between the blood and the tissues. The endothelium also produces molecules that discourage the blood from clotting unless there is a leak. Pericyte cells can contract and decrease the size of the arterioles and thereby regulate blood flow and blood pressure.
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The efferent arterioles of the juxtamedullary glomeruli are much different. They do break up, but they form bundles of vessels (arteriolae recti) that cross the outer zone of the medulla to perfuse the inner zone. Vessels returning from the inner medulla (venulae recti) intersperse themselves in a highly regular fashion among the descending arteriolae recti to form a well- organized rete mirabile. This rete is responsible for the osmotic isolation of the inner medulla from the rest of the kidney and so permits the excretion of a hypertonic urine when circumstances require.
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Mesangial cells form a glomerular functional unit with glomerular endothelial cells and podocytes through interactions of molecular signalling pathways which are essential for the formation of the glomerular tuft. Mesangial cells aid filtration by constituting part of the glomerular capillary tuft structure that filters fluids to produce urine. Communication between mesangial cells and vascular smooth muscle cells via gap junctions helps regulate the process of tubuloglomerular feedback and urine formation. Damage to mesangial cells using Thy 1-1 antibody specific to mesangial cells causes the vasoconstriction of arterioles mediated by tubuloglomerular feedback to be lost.
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There are five types of blood vessels: the arteries, which carry the blood away from the heart; the arterioles; the capillaries, where the exchange of water and chemicals between the blood and the tissues occurs; the venules; and the veins, which carry blood from the capillaries back towards the heart. The word vascular, meaning relating to the blood vessels, is derived from the Latin vas, meaning vessel. Some structures – such as cartilage, the epithelium, and the lens and cornea of the eye – do not contain blood vessels and are labeled avascular.
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Specifically within and between the pituitary lobes is anatomical evidence for confluent interlobe venules providing blood from the anterior to the neural lobe that would facilitate moment-to-moment sharing of information between lobes of the pituitary gland. In contrast to regular venules, high endothelial venules are a special type of venule where the endothelium is made up of simple cuboidal cells. Lymphocytes exit the blood stream and enter the lymph nodes via these specialized venules when an infection is detected. Compared with arterioles, the venules are larger with much weaker muscular coat.
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The structure of the tunica intima depends on the blood vessel type. Elastic arteries – A single layer of epithelial cells and a supporting layer of elastin-rich collagen. The layer also contains fibroblasts and smooth muscle cells called 'myointimal cells' Muscular arteries – Endothelial cells Arterioles – A single layer of epithelial cells Veins – Endothelial cells The inner coat consists of: # A layer of pavement endothelium, the cells of which are polygonal, oval, or fusiform, and have very distinct round or oval nuclei. This endothelium is brought into view most distinctly by staining with silver nitrate.
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A muscular artery (or distributing artery) is a medium-sized artery that draws blood from an elastic artery and branches into "resistance vessels" including small arteries and arterioles. Their walls contain larger number of smooth muscles, allowing them to contract and expand depending on peripheral blood demand . This contrasts to the mechanism of elastic arteries, which use their elastic properties to store the energy generated by the heart's contraction for a brief moment (elastic recoil). Under the microscope, muscular arteries can be identified by their clearly defined internal elastic lamina.
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These collect in progressively larger veins until they reach the body's two largest veins, the superior and inferior vena cava, which drain blood into the right side of the heart. From here, the blood is pumped into the lungs where it receives oxygen and drains back into the left side of the heart. From here, it is pumped into the body's largest artery, the aorta, and then progressively smaller arteries and arterioles until it reaches tissue. Here blood passes from small arteries into capillaries, then small veins and the process begins again.
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Livedo reticularis is a common skin finding consisting of a mottled reticulated vascular pattern that appears as a lace-like purplish discoloration of the skin. The discoloration is caused by reduction in blood flow through the arterioles that supply the cutaneous capillaries, resulting in deoxygenated blood showing as blue discoloration. This can be a secondary effect of a condition that increases a person's risk of forming blood clots, including a wide array of pathological and nonpathological conditions. Examples include hyperlipidemia, microvascular hematological or anemia states, nutritional deficiencies, hyper- and autoimmune diseases, and drugs/toxins.
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The macula densa is a collection of densely packed epithelial cells at the junction of the thick ascending limb (TAL) and distal convoluted tubule (DCT). As the TAL ascends through the renal cortex, it encounters its own glomerulus, bringing the macula densa to rest at the angle between the afferent and efferent arterioles. The macula densa's position enables it to rapidly alter afferent arteriolar resistance in response to changes in the flow rate through the distal nephron. The macula densa uses the composition of the tubular fluid as an indicator of GFR.
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When the cell swells, ATP escapes through a basolateral, stretch-activated, non-selective Maxi-Anion channel. The ATP is subsequently converted to adenosine by ecto-5′-nucleotidase. # Adenosine constricts the afferent arteriole by binding with high affinity to the A1 receptors a Gi/Go. Adenosine binds with much lower affinity to A2A and A2B receptors causing dilation of efferent arterioles. #The binding of adenosine to the A1 receptor causes a complex signal cascade involving the Gi subunit deactivating Ac, thus reducing cAMP and the Go subunit activating PLC, IP3 and DAG.
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Second-impact syndrome, in which the brain swells dangerously after a minor blow, may occur in very rare cases. The condition may develop in people who receive second blow days or weeks after an initial concussion before its symptoms have gone away. No one is certain of the cause of this often fatal complication, but it is commonly thought that the swelling occurs because the brain's arterioles lose the ability to regulate their diameter, causing a loss of control over cerebral blood flow. As the brain swells, intracranial pressure rapidly rises.
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Blood exits the glomerular capillaries by an efferent arteriole instead of a venule, as is seen in the majority of capillary systems (Fig. 4). This provides tighter control over the blood flow through the glomerulus, since arterioles dilate and constrict more readily than venules, owing to their thick circular smooth muscle layer (tunica media). The blood exiting the efferent arteriole enters a renal venule, which in turn enters a renal interlobular vein and then into the renal vein. Cortical nephrons near the corticomedullary junction (15% of all nephrons) are called juxtamedullary nephrons.
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Lipohyalinosis is a cerebral small vessel disease affecting the small arteries, arterioles or capillaries in the brain. Originally defined by C. Miller Fisher as 'segmental arteriolar wall disorganisation', it is characterized by vessel wall thickening and a resultant reduction in luminal diameter. Fisher considered this small vessel disease to be the result of hypertension, induced in the acute stage by fibrinoid necrosis that would lead to occlusion and hence lacunar stroke. However, recent evidence suggests that endothelial dysfunction as a result of inflammation is a more likely cause for it.
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The increased peripheral resistance in established hypertension is mainly attributable to structural narrowing of small arteries and arterioles, although a reduction in the number or density of capillaries may also contribute. It is not clear whether or not vasoconstriction of arteriolar blood vessels plays a role in hypertension. Hypertension is also associated with decreased peripheral venous compliance which may increase venous return, increase cardiac preload and, ultimately, cause diastolic dysfunction. Pulse pressure (the difference between systolic and diastolic blood pressure) is frequently increased in older people with hypertension.
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There are four subtypes of the CRH receptor known at present, defined as CRF-1, CRF-2a, CRF-2b, and CRF-2g. Three of these receptors are expressed only in the brain: CRF-1 in the cortex and cerebrum, CRF-2a in the lateral septum and hypothalamus, and CRF-2g in the amygdala. CRF-2b is expressed in the choroid plexus and cerebral arterioles in the brain, but is expressed mainly peripherally on the heart and skeletal muscle tissue. Extensive research has shown that overactivity in the brain CRF-CRF1 signaling system contributes to the onset of anxiety disorders and depression.
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Cerebral atherosclerosis is a type of atherosclerosis where build-up of plaque in the blood vessels of the brain occurs. Some of the main components of the plaques are connective tissue, extracellular matrix, including collagen, proteoglycans, fibronectin, and elastic fibers; crystalline cholesterol, cholesteryl esters, and phospholipids; cells such as monocyte derived macrophages, T-lymphocytes, and smooth muscle cells. The plaque that builds up can lead to further complications such as stroke, as the plaque disrupts blood flow within the intracranial arterioles. This causes the downstream sections of the brain that would normally be supplied by the blocked artery to suffer from ischemia.
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However, this assumption fails when considering forward flow within arterioles. At the microscopic scale, the effects of individual red blood cells become significant, and whole blood can no longer be modeled as a continuum. When the diameter of the blood vessel is just slightly larger than the diameter of the red blood cell the Fahraeus–Lindquist effect occurs and there is a decrease in wall shear stress. However, as the diameter of the blood vessel decreases further, the red blood cells have to squeeze through the vessel and often can only pass in a single file.
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Henoch–Schönlein purpura is a small-vessel vasculitis in which complexes of immunoglobulin A (IgA) and complement component 3 (C3) are deposited on arterioles, capillaries, and venules (hence it is a type III hypersensitivity reaction). As with IgA nephropathy, serum levels of IgA are high in HSP and there are identical findings on renal biopsy; however, IgA nephropathy has a predilection for young adults while HSP is more predominant among children. Further, IgA nephropathy typically only affects the kidneys while HSP is a systemic disease. HSP involves the skin and connective tissues, scrotum, joints, gastrointestinal tract and kidneys.
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In some very aerobically athletic individuals, for example distance runners, the diastolic will progressively fall as the systolic increases. This behavior facilitates a much greater increase in stroke volume and cardiac output at a lower mean arterial pressure and enables much greater aerobic capacity and physical performance. The diastolic drop reflects a much greater fall in systemic vascular resistance of the muscle arterioles in response to the exercise (a greater proportion of red versus white muscle tissue). Individuals with larger BMIs due to increased muscle mass (bodybuilders) have also been shown to have lower diastolic pressures and larger pulse pressures.
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20-HETE-synthesizng enzymes are widely distributed to liver, kidney, brain, lung, intestine and blood vessels. In most vascular systems, 20-HETE synthesizing activity is limited to vascular smooth muscle of small blood vessels with little or no such activity in the vessel's endothelial cells or in large blood vessels. However, both the smooth muscle and endothelial cells obtained from mouse brain microvasculature, produce 20-HETE in culture. 20-HETE is produced by human neutrophils and platelets and by the ascending tubule cells in the medulla as well the pre-glomerular arterioles and certain other localized areas of the rabbit kidney.
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Staging of chronic kidney disease is based on categories of GFR as well as albuminuria and cause of kidney disease. Central to the physiologic maintenance of GFR is the differential basal tone of the afferent and efferent arterioles (see diagram). In other words, the filtration rate is dependent on the difference between the higher blood pressure created by vasoconstriction of the input or afferent arteriole versus the lower blood pressure created by lesser vasoconstriction of the output or efferent arteriole. GFR is equal to the renal clearance ratio when any solute is freely filtered and is neither reabsorbed nor secreted by the kidneys.
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Bradykinin (Greek brady-, slow; -kinin, kīn(eîn) to move) is a peptide that promotes inflammation. It causes arterioles to dilate (enlarge) via the release of prostacyclin, nitric oxide, and endothelium-derived hyperpolarizing factor and makes veins constrict, via prostaglandin F2, thereby leading to leakage into capillary beds, due to the increased pressure in the capillaries. Bradykinin is a physiologically and pharmacologically active peptide of the kinin group of proteins, consisting of nine amino acids. A class of drugs called angiotensin converting enzyme inhibitors (ACE inhibitors) increase bradykinin levels by inhibiting its degradation, thereby increasing its blood pressure lowering effect.
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In the short-term, the greater the blood volume, the higher the cardiac output. This has been proposed as an explanation of the relationship between high dietary salt intake and increased blood pressure; however, responses to increased dietary sodium intake vary between individuals and are highly dependent on autonomic nervous system responses and the renin–angiotensin system, changes in plasma osmolarity may also be important. In the longer-term the relationship between volume and blood pressure is more complex. In simple terms systemic vascular resistance is mainly determined by the caliber of small arteries and arterioles.
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Conventional methods used to examine intrinsic properties of isolated resistance vessels (arterioles and small arteries with diameters varying between 30 µm and 300 µm) include the pressure myography technique. However, such methods currently require manually skilled personnel and are not scalable. An artery-on-a-chip could overcome several of these limitations by accommodating an artery onto a platform which would be scalable, inexpensive and possibly automated in its manufacturing. An organ-based microfluidic platform has been developed as a lab-on-a-chip onto which a fragile blood vessel can be fixed, allowing for determinants of resistance artery malfunctions to be studied.
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Birds have a very efficient system for diffusing oxygen into the blood; birds have a ten times greater surface area to gas exchange volume than mammals. As a result, birds have more blood in their capillaries per unit of volume of lung than a mammal. The arteries are composed of thick elastic muscles to withstand the pressure of the ventricular contractions, and become more rigid as they move away from the heart. Blood moves through the arteries, which undergo vasoconstriction, and into arterioles which act as a transportation system to distribute primarily oxygen as well as nutrients to all tissues of the body.
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EP3 is widely distributed in humans. Its protein and/or mRNA is expressed in kidney (i.e. glomeruli, Tamm-Horsfall protein negative late distal convoluted tubules, connecting segments, cortical and medullary collecting ducts, media and endothelial cells of arteries and arterioles); stomach (vascular smooth muscle and gastric fundus mucosal cells); thalamus (anterior, ventromedial, laterodorsal, paraventricular and central medial nuclei); intestinal mucosal epithelia at the apex of crypts; myometrium (stromal cells, endothelial cells, and, in pregnancy, placenta, chorion, and amnion); mouth gingival fibroblasts; and eye (corneal endothelium and keratocytes, trabecular cells, ciliary epithelium, and conjunctival and iridal stroma cells, and retinal Müller cells).
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Although the structure and function is basically the same in smooth muscle cells in different organs, their specific effects or end-functions differ. The contractile function of vascular smooth muscle regulates the lumenal diameter of the small arteries- arterioles called resistance vessels, thereby contributing significantly to setting the level of blood pressure and blood flow to vascular beds. Smooth muscle contracts slowly and may maintain the contraction (tonically) for prolonged periods in blood vessels, bronchioles, and some sphincters. Activating arteriole smooth muscle can decrease the lumenal diameter 1/3 of resting so it drastically alters blood flow and resistance.
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Second-impact syndrome (SIS) occurs when the brain swells rapidly, and catastrophically, after a person suffers a second concussion before symptoms from an earlier one have subsided. This second blow may occur minutes, days or weeks after an initial concussion, and even the mildest grade of concussion can lead to SIS. The condition is often fatal, and almost everyone who is not killed is severely disabled. The cause of SIS is uncertain, but it is thought that the brain's arterioles lose their ability to regulate their diameter, and therefore lose control over cerebral blood flow, causing massive cerebral edema.
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Some common dose-dependent adverse effects of amlodipine include vasodilatory effects, peripheral edema, dizziness, palpitations, and flushing. Peripheral edema (fluid accumulation in the tissues) occurs at rate of 10.8% at a 10-mg dose (versus 0.6% for placebos), and is three times more likely in women than in men. It causes more dilation in the arterioles and precapillary vessels than the postcapillary vessels and venules. The increased dilation allows for more blood, which is unable to push through to the relatively constricted postcapillary venules and vessels; the pressure causes much of the plasma to move into the interstitial space.
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In the kidneys, as a result of benign arterial hypertension, hyaline (pink, amorphous, homogeneous material) accumulates in the walls of small arteries and arterioles, producing the thickening of their walls and the narrowing of the arterial openings, a process known as arteriolosclerosis. The resulting inadequate blood flow produces tubular atrophy, interstitial fibrosis, and glomerular alterations (smaller glomeruli with different degrees of hyalinization – from mild to sclerosis of glomeruli) and scarring around the glomeruli (periglomerular fibrosis). In advanced stages, kidney failure will occur. Functional nephrons have dilated tubules, often with hyaline casts in the opening of the tubules.
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Reperfusion of ischemic tissues is often associated with microvascular injury, particularly due to increased permeability of capillaries and arterioles that lead to an increase of diffusion and fluid filtration across the tissues. Activated endothelial cells produce more reactive oxygen species but less nitric oxide following reperfusion, and the imbalance results in a subsequent inflammatory response. The inflammatory response is partially responsible for the damage of reperfusion injury. White blood cells, carried to the area by the newly returning blood, release a host of inflammatory factors such as interleukins as well as free radicals in response to tissue damage.
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The enzyme renin is secreted by pericytes (mural cells) (1) in the vicinity of the afferent arterioles and similar microvessels of the kidney from specialized cells of the juxtaglomerular apparatus—the juxtaglomerular cells, in response to three stimuli: # A decrease in arterial blood pressure (that could be related to a decrease in blood volume) as detected by baroreceptors (pressure-sensitive cells). This is the most direct causal link between blood pressure and renin secretion (the other two methods operate via longer pathways). # A decrease in sodium load delivered to the distal tubule. This load is measured by the macula densa of the juxtaglomerular apparatus.
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When angiotensin II levels are increased due to activation of the renin–angiotensin–aldosterone system, most of the arteries in the body experience vasoconstriction, in order to maintain adequate blood pressure. However, this reduces blood flow to the kidneys. To compensate, the efferent arterioles constrict to a greater degree than the other arteries, in response to increased levels of angiotensin II. Pressure in glomerular capillaries is therefore maintained and glomerular filtration rate remains adequate. However, in states of where angiotensin II is very high for a prolonged period of time, the colloid oncotic pressure of the capillaries will increase, counteracting the increased hydrostatic pressure from the efferent constriction.
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The arcuate vessels of the uterus are a component of the blood supply of the uterus. They are arteries and veins that branch from the uterine arteries and veins, respectively, with additional anastomoses from the ovarian arteries and veins,Bottom of page 123 in: and penetrate and assume a circumferential course in the myometrium.Page 440 - section Uterus in: They have also been called helicine branches of the uterus (or helicine arterioles), as they are spiral-shaped, but they should not be confused with the spiral arteries that penetrate the endometrium in the inner uterus. The radial arteries branch off from the arcuate artery through the myometrium.
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The classical explanation of HPV involves inhibition of hypoxia-sensitive voltage-gated potassium channels in pulmonary artery smooth muscle cells leading to depolarization. This depolarization activates voltage-dependent calcium channels, which increases intracellular calcium and activates smooth muscle contractile machinery which in turn causes vasoconstriction. However, later studies have reported additional ion channels and mechanisms that contribute to HPV, such as transient receptor potential canonical 6 (TRPC6) channels, and transient receptor potential vanilloid 4 (TRPV4) channels. Recently it was proposed that hypoxia is sensed at the alveolar/capillary level, generating an electrical signal that is transduced to pulmonary arterioles through gap junctions in the pulmonary endothelium to cause HPV.
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The latter is the most important variable in determining resistance, with the TPR changing by the fourth power of the radius. An increase in either of these physiological components (cardiac output or TPR) causes a rise in the mean arterial pressure. Vasodilation works to decrease TPR and blood pressure through relaxation of smooth muscle cells in the tunica media layer of large arteries and smaller arterioles. Vasodilation occurs in superficial blood vessels of warm-blooded animals when their ambient environment is hot; this process diverts the flow of heated blood to the skin of the animal, where heat can be more easily released to the atmosphere.
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The activation of platelets resulting from inhibition of ADAMTS13 is due to the hyperactivity of large multimers of uncleaved vWF. The arterioles and capillaries of the body become obstructed by the resulting complexes of activated platelets, which have adhered to the endothelium via large multimeric vWF. Through a mechanism known as microangiopathic hemolysis, the growing thrombi lodged in smaller vessels destroy red blood cells (RBCs) as they squeeze through the narrowed blood vessels, forming schistocytes, or fragments of sheared RBCs. The presence of schistocytes is a key finding that helps to diagnose HUS. Typically, this hemolysis results in a hemoglobin level of less than 80 g/L.
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The resistance attributable to a blood vessel depends on its radius as described by the Hagen-Poiseuille's equation (resistance∝1/radius4). Hence, the smaller the radius, the higher the resistance. Other physical factors that affect resistance include: vessel length (the longer the vessel, the higher the resistance), blood viscosity (the higher the viscosity, the higher the resistance) and the number of vessels, particularly the smaller numerous, arterioles and capillaries. The presence of a severe arterial stenosis increases resistance to flow, however this increase in resistance rarely increases systemic blood pressure because its contribution to total systemic resistance is small, although it may profoundly decrease downstream flow.
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Adults of E. sagitta have been found attached to the inner walls of the chambers and vessels of the heart, as well as the arterioles of the lungs of various hosts: Bushbuck (Tragelaphus scriptus), Greater kudu (Tragelaphus strepsiceros), bongos (Tragelaphus eurycerus), nyala (Tragelaphus angasii), common eland (Taurotragus oryx), and African Forest Buffalo (Syncerus caffer nanus). This species has also been found in unspecified "cattle". Lesions similar to those described in E. sagitta infestations were also found in sheep (Ovis aries), but the actual parasites were not recovered. E. sagitta has been found in several African nations: Cameroon, Kenya, Malawi, Mocambique, the Republic of the Congo, South Africa and Swaziland.
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There are numerous thermal effectors including sweat glands, smooth muscles of blood vessels, some endocrine glands, and skeletal muscle. With an increase in the core temperature, the thermal regulatory center will stimulate the arterioles supplying blood to the skin to dilate along with the release of sweat on the skin surface to reduce temperature through evaporation. In addition to the involuntary regulation of temperature, the hypothalamus is able to communicate with the cerebral cortex to initiate voluntary control such as removing clothing or drinking cold water. With all regulations taken into account, the body is able to maintain core temperature within about two or three degrees Celsius during exercise.
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Neurons are the excitable cells that process and transmit these reflex signals through their axons, dendrites, and cell bodies. Axons directly facilitate intercellular communication projecting from the neuronal cell body to other neurons, local muscle tissue, glands and arterioles. In the axon reflex, signaling starts in the middle of the axon at the stimulation site and transmits signals directly to the effector organ skipping both an integration center and a chemical synapse present in the spinal cord reflex. The impulse is limited to a single bifurcated axon, or a neuron whose axon branches into two divisions and does not cause a general response to surrounding tissue.
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However, the subsequent hyperpolarization (IPSP) and slow depolarization (Slow EPSP) that represent the recovery of the postganglionic neuron from stimulation are actually mediated by muscarinic receptors, types M2 and M1 respectively (discussed below). Peripheral autonomic fibers (sympathetic and parasympathetic fibers) are categorized anatomically as either preganglionic or postganglionic fibers, then further generalized as either adrenergic fibers, releasing noradrenaline, or cholinergic fibers, both releasing acetylcholine and expressing acetylcholine receptors. Both preganglionic sympathetic fibers and preganglionic parasympathetic fibers are cholinergic. Most postganglionic sympathetic fibers are adrenergic: their neurotransmitter is norepinephrine except postganglionic sympathetic fibers to the sweat glands, piloerectile muscles of the body hairs, and the skeletal muscle arterioles do not use adrenaline/noradrenaline.
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19-HETE is an inhibitor of 20-HETE, a broadly active signaling molecule which acts to onstrict arterioles, elevate blood pressure, promote inflammation responses, and stimulates the growth of various types of tumor cells; however the in vivo ability and significance of 19-HETE in inhibiting 20-HETE has not been demonstrated (see 20-Hydroxyeicosatetraenoic acid). The EDPs (see Epoxydocosapentaenoic acid) and EEQs (see epoxyeicosatetraenoic acid) have a broad range of activities. In various animal models and in vitro studies on animal and human tissues, they decrease hypertension and pain perception; suppress inflammation; inhibit angiogenesis, endothelial cell migration and endothelial cell proliferation; and inhibit the growth and metastasis of human breast and prostate cancer cell lines.
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Lisinopril is an ACE inhibitor, meaning it blocks the actions of angiotensin-converting enzyme (ACE) in the renin–angiotensin–aldosterone system (RAAS), preventing angiotensin I from being converted to angiotensin II. Angiotensin II is a potent direct vasoconstrictor and a stimulator of aldosterone release. Reduction in the amount of angiotensin II results in relaxation of the arterioles. Reduction in the amount of angiotensin II also reduces the release of aldosterone from the adrenal cortex, which allows the kidney to excrete sodium along with water into the urine, and increases retention of potassium ions. Specifically, this process occurs in the peritubular capillaries of the kidneys in response to a change in Starling forces.
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In the kidneys, blocking of N-type calcium channels reduce glomerular pressure through dilation of arterioles. N-type calcium channels have been shown to play a part in the localization of neurite growth in the sympathetic nervous system and the skin and spinal cord. The neurite outgrowth was shown to be inhibited through an interaction between laminin and the 11th loop of the n-type calcium channel structure. It has been suggested that neurites outgrowth is inhibited by the influx of calcium through the growth cone, and this happens when the Cav2.2 channel comes in contact with laminin 2, and in response can induce a stretch activation of the N-type calcium channel.
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The very smallest distal branches anastomose through the skull with small arterioles from the scalp. On entering the cranium, the middle meningeal artery gives off the following branches: # Numerous small vessels supply the trigeminal ganglion and the dura mater # A superficial petrosal branch enters the hiatus of the facial canal, supplies the facial nerve, and anastomoses with the stylomastoid branch of the posterior auricular artery. # A superior tympanic artery runs in the canal of the tensor tympani muscle, and supplies this muscle and the lining of the canal. # Orbital branches pass through the superior orbital fissure or through separate canals in the great wing of the sphenoid, to anastomose with the lacrimal or other branches of the ophthalmic artery.
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Grossly, LAM lungs are enlarged and diffusely cystic, with dilated air spaces as large as several centimeters in diameter. Microscopic examination of the lung reveals foci of smooth muscle-like cell infiltration of the lung parenchyma, airways, lymphatics, and blood vessels associated with areas of thin-walled cystic change. LAM lesions often contain an abundance of lymphatic channels, forming an anastomosing meshwork of slit-like spaces lined by endothelial cells. LAM cells generally expand interstitial spaces without violating tissue planes but have been observed to invade the airways, the pulmonary artery, the diaphragm, aorta, and retroperitoneal fat, to destroy bronchial cartilage and arteriolar walls, and to occlude the lumen of pulmonary arterioles.
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19-HETE is an inhibitor of 20-HETE, a broadly active signaling molecule, e.g. it constricts arterioles, elevates blood pressure, promotes inflammation responses, and stimulates the growth of various types of tumor cells; however the in vivo ability and significance of 19-HETE in inhibiting 20-HETE has not been demonstrated (see 20-Hydroxyeicosatetraenoic acid). The EDP (see Epoxydocosapentaenoic acid) and EEQ (see epoxyeicosatetraenoic acid) metabolites have a broad range of activities. In various animal models and in vitro studies on animal and human tissues, they decrease hypertension and pain perception; suppress inflammation; inhibit angiogenesis, endothelial cell migration and endothelial cell proliferation; and inhibit the growth and metastasis of human breast and prostate cancer cell lines.
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Melanin is produced within the skin in cells called melanocytes and it is the main determinant of the skin color of darker-skin humans. The skin color of people with light skin is determined mainly by the bluish-white connective tissue under the dermis and by the hemoglobin circulating in the veins of the dermis. The red color underlying the skin becomes more visible, especially in the face, when, as consequence of physical exercise or the stimulation of the nervous system (anger, fear), arterioles dilate. Color is not entirely uniform across an individual's skin; for example, the skin of the palm and the sole is lighter than most other skin, and this is especially noticeable in darker-skinned people.
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LECT2 amyloidosis is diagnosed by a kidney biopsy which reveals two key findings: a) histological evidence of Congo red staining material deposited in the interstitial, mesangial, glomerular, and/or vascular areas of the kidney and b) the identification of these deposits as containing mainly LECT2 as identified by proteomics methodologies. Kidney biopsy shows the presence of LECT2-based amyloid predominantly in the renal cortex interstitium, glomeruli, and arterioles. LECT2 amyloidosis can be distinguished from AL amyloidosis, the most common form of amyloidosis (~85% of total cases), by testing their blood for the presence of high levels of a clonal immunoglobulin light chain. If the patient tests negative for this light chain, positive Congo Red staining of the kidney biopsy strongly suggests LECT2 amyloidosis.
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Cilnidipine decreases blood pressure and is used to treat hypertension and its comorbidities. Due to its blocking action at the N-type and L-type calcium channel, cilnidipine dilates both arterioles and venules, reducing the pressure in the capillary bed. Cilnidipine is vasoselective and has a weak direct dromotropic effect, a strong vasodepressor effect, and an arrhythmia-inhibiting effect. Blood pressure control with cilnidipine treatment in Japanese post-stroke hypertensive patients [The CA-ATTEND study] - the results of a large-scale prospective post-marketing surveillance study of post-stroke hypertensive patients (n = 2667, male 60.4%, 69.0 ± 10.9 years) treated with cilnidipine indicate that cilnidipine was effective in treating uncontrolled blood pressure and was well tolerated in post-stroke hypertensive patients.
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Blood pressure in the arteries supplying the body is a result of the work needed to pump the cardiac output (the flow of blood pumped by the heart) through the vascular resistance, usually termed total peripheral resistance by physicians and researchers. An increase in the media to lumenal diameter ratio has been observed in hypertensive arterioles (arteriolosclerosis) as the vascular wall thickens and/or lumenal diameter decreases. The up and down fluctuation of the arterial blood pressure is due to the pulsatile nature of the cardiac output and determined by the interaction of the stroke volume versus the volume and elasticity of the major arteries. The decreased velocity of flow in the capillaries increases the blood pressure, due to Bernoulli's principle.
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The underlying mechanism typically involves autoantibody-mediated inhibition of the enzyme ADAMTS13, a metalloprotease responsible for cleaving large multimers of von Willebrand factor (vWF) into smaller units. The increase in circulating multimers of vWF increases platelet adhesion to areas of endothelial injury, particularly where arterioles and capillaries meet, which in turn results in the formation of small platelet clots called thrombi. As platelets are used up in the formation of thrombi, this then leads to a decrease in the number of overall circulating platelets, which may then cause life-threatening bleeds. Red blood cells passing the microscopic clots are subjected to shear stress, which damages their membranes, leading to rupture of red blood cells within blood vessels, which in turn leads to anaemia and schistocyte formation.
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Increasing evidence suggests that pericytes can regulate blood flow at the capillary level. For the retina, movies have been published showing that pericytes constrict capillaries when their membrane potential is altered to cause calcium influx, and in the brain it has been reported that neuronal activity increases local blood flow by inducing pericytes to dilate capillaries before upstream arteriole dilation occurs. This area is controversial, with a recent study claiming that pericytes do not express contractile proteins and are not capable of contraction in vivo, although the latter paper has been criticised for using a highly unconventional definition of pericyte which explicitly excludes contractile pericytes. It appears that different signaling pathways regulate the constriction of capillaries by pericytes and of arterioles by smooth muscle cells.
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With the exception of pulmonary and umbilical arteries and their corresponding veins, arteries carry oxygenated blood away from the heart and deliver it to the body via arterioles and capillaries, where the oxygen is consumed; afterwards, venules and veins carry deoxygenated blood back to the heart. Under normal conditions in adult humans at rest, hemoglobin in blood leaving the lungs is about 98–99% saturated with oxygen, achieving an oxygen delivery between 950 and 1150 ml/minEdwards Lifesciences LLC – Normal Hemodynamic Parameters – Adult 2009 to the body. In a healthy adult at rest, oxygen consumption is approximately 200–250 ml/min, and deoxygenated blood returning to the lungs is still roughly 75%Transplant Support- Lung, Heart/Lung, Heart MSN groups (70 to 78%) saturated.
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Chemical structure of sildenafil (Viagra), the prototypical PDE5 inhibitor A phosphodiesterase type 5 inhibitor (PDE5 inhibitor) is a drug used to block the degradative action of cGMP-specific phosphodiesterase type 5 (PDE5) on cyclic GMP in the smooth muscle cells lining the blood vessels supplying various tissues. These drugs dilate the corpora cavernosa of the penis, facilitating erection with sexual stimulation, and are used in the treatment of erectile dysfunction (ED). Sildenafil was the first effective oral treatment available for ED. Because PDE5 is also present in the smooth muscle of the walls of the arterioles within the lungs, sildenafil and tadalafil dilates those vessels, and are FDA-approved for the treatment of pulmonary hypertension. Increasingly, the wider cardiovascular benefits of PDE5 inhibitors are being appreciated.
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The myogenic mechanism is how arteries and arterioles react to an increase or decrease of blood pressure to keep the blood flow within the blood vessel constant. Myogenic response refers to a contraction initiated by the myocyte itself instead of an outside occurrence or stimulus such as nerve innervation. Most often observed in (although not necessarily restricted to) smaller resistance arteries, this 'basal' tone may be useful in the regulation of organ blood flow and peripheral resistance, as it positions a vessel in a preconstricted state that allows other factors to induce additional constriction or dilation to increase or decrease blood flow. The smooth muscle of the blood vessels reacts to the stretching of the muscle by opening ion channels, which cause the muscle to depolarize, leading to muscle contraction.
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The unraveling of high molecular weight von Willebrand factor in conditions of high shear stress is essential in the prevention of bleeding in the vasculature of the gastrointestinal system where small arterioles are common, as platelets cannot bind to damaged blood vessel walls well in such conditions. This is particularly true in the presence of intestinal angiodysplasia, where arteriovenous malformations lead to very high blood flow, and so the loss of von Willebrand factor can lead to much more extensive bleeding from these lesions. When people with aortic stenosis also have gastrointestinal bleeding, it is invariably from angiodysplasia. It has been hypothesized that defects in high molecular weight von Willebrand factor could actually be the cause of the arteriovenus malformations in intestinal angiodysplasia, rather than just making existing angiodysplasic lesions bleed.
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Cerebral vasculitis (sometimes the word angiitis is used instead of "vasculitis") is vasculitis (inflammation of the blood vessel wall) involving the brain and occasionally the spinal cord. It affects all of the vessels: very small blood vessels (capillaries), medium-size blood vessels (arterioles and venules), or large blood vessels (arteries and veins). If blood flow in a vessel with vasculitis is reduced or stopped, the parts of the body that receive blood from that vessel begins to die. It may produce a wide range of neurological symptoms, such as headache, skin rashes, feeling very tired, joint pains, difficulty moving or coordinating part of the body, changes in sensation, and alterations in perception, thought or behavior, as well as the phenomena of a mass lesion in the brain leading to coma and herniation.
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There are two variants of retinal vessel analysis which are based on a special fundus camera, the Retinal Vessel Analyzer which was developed by Imedos, a medical engineering company in Jena, Germany. Basically, the Retinal Vessel Analyzer measures the diameters of small arteries (arterioles) and vein (venules) in the posterior segment of the eye. In static retinal vessel analysis this is a snapshot, in dynamic vessel analysis (DVA) a 12.5 Hz optoelectric flickering light induces a stimulation of a specific segment of the retina to which the vessels react by a change in their diameter which is quantified by the device. There are different protocols for conducting this examination; a typical procedure consists of applying flicker light three times over 20 seconds each, followed by 80 seconds relaxation time.
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Multiunit smooth muscle tissues innervate individual cells; as such, they allow for fine control and gradual responses, much like motor unit recruitment in skeletal muscle. Smooth muscle is found within the walls of blood vessels (such smooth muscle specifically being termed vascular smooth muscle) such as in the tunica media layer of large (aorta) and small arteries, arterioles and veins. Smooth muscle is also found in lymphatic vessels, the urinary bladder, uterus (termed uterine smooth muscle), male and female reproductive tracts, gastrointestinal tract, respiratory tract, arrector pili of skin, the ciliary muscle, and iris of the eye. The structure and function is basically the same in smooth muscle cells in different organs, but the inducing stimuli differ substantially, in order to perform individual effects in the body at individual times.
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Angiotensin II also acts on the smooth muscle in the walls of the arterioles causing these small diameter vessels to constrict, thereby restricting the outflow of blood from the arterial tree, causing the arterial blood pressure to rise. This, therefore, reinforces the measures described above (under the heading of "Arterial blood pressure"), which defend the arterial blood pressure against changes, especially hypotension. The angiotensin II-stimulated aldosterone released from the zona glomerulosa of the adrenal glands has an effect on particularly the epithelial cells of the distal convoluted tubules and collecting ducts of the kidneys. Here it causes the reabsorption of sodium ions from the renal tubular fluid, in exchange for potassium ions which are secreted from the blood plasma into the tubular fluid to exit the body via the urine.
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The concentration of pheomelanin varies highly within populations from individual to individual, but it is more commonly found among lightly pigmented Europeans, East Asians, and Native Americans. For the same body region, individuals, independently of skin colour, have the same amount of melanocytes (however variation between different body parts is substantial), but organelles which contain pigments, called melanosomes, are smaller and less numerous in light-skinned humans. For people with very light skin, the skin gets most of its colour from the bluish- white connective tissue in the dermis and from the haemoglobin associated blood cells circulating in the capillaries of the dermis. The colour associated with the circulating haemoglobin become more obvious, especially in the face, when arterioles dilate and become tumefied with blood as a result of prolonged physical exercise or stimulation of the sympathetic nervous system (usually embarrassment or anger).
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When looking at viscoelastic behavior of blood in vivo, it is necessary to also consider the effects of arteries, capillaries, and veins. The viscosity of blood has a primary influence on flow in the larger arteries, while the elasticity, which resides in the elastic deformability of red blood cells, has primary influence in the arterioles and the capillaries.A. Ündar, W. Vaughn, and J. Calhoon, The effects of cardiopulmonary bypass and deep hypothermic circulatory arrest on blood viscoelasticity and cerebral blood flow in a neonatal piglet model, Perfusion 2000, 15, 121–128 Understanding wave propagation in arterial walls, local hemodynamics, and wall shear stress gradient is important in understanding the mechanisms of cardiovascular function. Arterial walls are anisotropic and heterogeneous, composed of layers with different bio-mechanical characteristics which makes understanding the mechanical influences that arteries contribute to blood flow very difficult.
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According to Cannon, the emotion of fear working on the mind, which he terms the "sympathetic" or "sympathico-adrenal" division of the nervous system, causes a fall in blood pressure as brought on by "a reduction of the volume of circulating blood". Cannon explains the loss of blood volume by the constant injection of adrenaline into the small arterioles which constrict, preventing a proper flow of blood within the body and causing a drop in blood pressure. From there, the weak blood pressure prevents the sufficient circulation of the blood by damaging the heart and nerves responsible for the maintenance of the vessels which transport blood, thus making it harder for circulation to continue since the very organs necessary to maintain proper blood circulation are deteriorating. An accelerated heart rate then ensues, followed by rapid breathing.
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EP2 is widely distributed in humans. Its protein is expressed in human small intestine, lung, media of arteries and arterioles of the kidney, thymus, uterus, brain cerebral cortex, brain striatum, brain hippocampus, corneal epithelium, corneal choriocapillaries, Myometriuml cells, eosinophiles, sclera of the eye, articular cartilage, the corpus cavernosum of the penis, and airway smooth muscle cells; its mRNA is expressed in gingival fibroblasts, monocyte-derived dendritic cells, aorta, corpus cavernosum of the penis, articular cartilage, airway smooth muscle, and airway epithelial cells. In rats, the receptor protein and/or mRNA has been found in lung, spleen, intestine, skin, kidney, liver, long bones, and rather extensively throughout the brain and other parts of the central nervous system. EP2 expression in fibroblasts from the lungs of mice with bleomycin-induced pulmonary fibrosis and humans with Idiopathic pulmonary fibrosis is greatly reduced.
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A large sodium chloride concentration is indicative of an elevated GFR, while low sodium chloride concentration indicates a depressed GFR. Sodium chloride is sensed by the macula densa mainly by an apical Na-K-2Cl cotransporter (NKCC2). The relationship between the TGF and NKCC2 can be seen through the administration of loop diuretics like furosemide. Furosemide blocks NaCl reabsorption mediated by the NKCC2 at the macula densa, which leads to increased renin release. Excluding loop diuretic use, the usual situation that causes a reduction in reabsorption of NaCl via the NKCC2 at the macula densa is a low tubular lumen concentration of NaCl. Reduced NaCl uptake via the NKCC2 at the macula densa leads to increased renin release, which leads to restoration of plasma volume, and to dilation of the afferent arterioles, which leads to increased renal plasma flow and increased GFR.
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Royal College of Surgeons of England, where Collier did his early research He interspersed his junior medical training with two days a week at a laboratory situated in the Royal College of Surgeons in Lincoln's Inn Fields, run by John Vane. In 1969, Collier confirmed, with Dornhorst, Lands' findings of β1-receptors in the heart and β2-receptors in the airways, in humans, and "suggested that the respiratory stimulation produced in man by β-receptor stimulants is a β 1 action and is not linked with bronchodilatation." In 1971, he co-authored a paper with Rod Flower showing that therapeutic doses of aspirin reduced prostaglandin E and F in human semen. His early research included looking at the veins of the back of the hand, and the behaviour of human peripheral blood vessels, being first to develop methods for studying how human veins respond to drugs and natural mediators in vivo and developed the idea that human veins and arterioles have very different pharmacologies.
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19-HETE is an inhibitor of 20-HETE, a broadly active signaling molecule which acts to onstrict arterioles, elevate blood pressure, promote inflammation responses, and stimulates the growth of various types of tumor cells; however the in vivo ability and significance of 19-HETE in inhibiting 20-HETE has not been demonstrated (see 20-Hydroxyeicosatetraenoic acid). The EDPs (see Epoxydocosapentaenoic acid) and EEQs (see epoxyeicosatetraenoic acid) have a broad range of activities. In various animal models and in vitro studies on animal and human tissues, they decrease hypertension and pain perception; suppress inflammation; inhibit angiogenesis, endothelial cell migration and endothelial cell proliferation; and inhibit the growth and metastasis of human breast and prostate cancer cell lines. It is suggested that the EDP and EEQ metabolites function in humans as they do in animal models and that, as products of the omega-3 fatty acids, DHA acid and EPA, the EDP and EEQ metabolites contribute to many of the beneficial effects attributed to dietary omega-3 fatty acids.
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High endothelial venules (HEV) are specialized post-capillary venous swellings characterized by plump endothelial cells as opposed to the usual thinner endothelial cells found in regular venules. HEVs enable lymphocytes circulating in the blood to directly enter a lymph node (by crossing through the HEV). Table 14-1 In humans, HEVs are found in all secondary lymphoid organs (with the exception of spleen, where blood exits through open arterioles and enters the red pulp), including hundreds of lymph nodes dispersed in the body, tonsils and adenoids in the pharynx, Peyer's patches (PIs) in the small intestine, appendix, and small aggregates of lymphoid tissue in the stomach and large intestine. In contrast to the endothelial cells from other vessels, the high endothelial cells of HEVs have a distinctive appearance, consisting of a cuboidal morphology and with various receptors to interact with leukocytes (express specialized ligands for lymphocytes and are able to support high levels of lymphocyte extravasation).
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Retinal vessel dynamics have the potential to serve as a tool for the assessment of risks in other organs since they are thought to reflect the general status of the microvasculature (i.e. the smallest vessels in the human body). The value of the examination with the Retinal Vessel Analyzer has been documented in a number of recent studies. There is growing evidence that in particular the dynamic vessel analysis is able to detect blood vessel damage - for instance as a consequence of aging or metabolic disease - in an early stage. Some examples: Cardiology In a recent publication, Andreas Flammer and his group at the Clinic of Cardiology at Zurich University performed retinal vessel analysis in 74 patients with compensated chronic heart failure, 74 patients with cardiovascular risk factors and 74 healthy controls. The primary endpoint, flicker-induced dilatation of retinal arterioles (FIDart), was significantly reduced in patients with chronic heart failure: 0.9% versus 2.3% in persons with risk factors and 3.6% in healthy individuals.
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EEQS, similar to EDPs, have not be studied nearly as well as the EETs. In comparison to the many activities attributed to the EETs in animal model studies (see Epoxyeicosatrienoic acid), a limited set of studies indicate that EEQs (and EPAs) mimic EETS in their abilities to dilate arterioles, reduce hypertension, inhibit inflammation (the anti-inflammatory actions of EEQ are less potent than those of the EETs) and thereby reduce occlusion of arteries to protect the heart and prevent and strokes (see Epoxyeicosatrienoic acid#Clinical significance sections on a) Regulation of blood pressure, b) Heart disease, c) Strokes and seizures, and d) inflammation); they also mimic EETs in possessing analgesia properties in relieving certain types of pain (see Epoxyeicosatrienoic acid#Clinical significance#Pain). Often, the EEQs (and EPAs) exhibit greater potency and/or effectiveness than EET in these actions. In human studies potentially relevant to one or more of these activities, consumption of long chain omega-3 fatty acid (i.e.
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Targeted deletion of Dicer in the FoxD1-derived renal progenitor cells in a murine model resulted in a complex renal phenotype including expansion of nephron progenitors, fewer renin cells, smooth muscle arterioles, progressive mesangial loss and glomerular aneurysms. High throughput whole transcriptome profiling of the FoxD1-Dicer knockout mouse model revealed ectopic upregulation of pro-apoptotic gene, Bcl2L11 (Bim) and dysregulation of the p53 pathway with increase in p53 effector genes including Bax, Trp53inp1, Jun, Cdkn1a, Mmp2, and Arid3a. p53 protein levels remained unchanged, suggesting that FoxD1 stromal miRNAs directly repress p53-effector genes. Using a lineage tracing approach followed by Fluorescent-activated cell sorting, miRNA profiling of the FoxD1-derived cells not only comprehensively defined the transcriptional landscape of miRNAs that are critical for vascular development, but also identified key miRNAs that are likely to modulate the renal phenotype in its absence. These miRNAs include miRs‐10a, 18a, 19b, 24, 30c, 92a, 106a, 130a, 152, 181a, 214, 222, 302a, 370, and 381 that regulate Bcl2L11 (Bim) and miRs‐15b, 18a, 21, 30c, 92a, 106a, 125b‐5p, 145, 214, 222, 296‐5p and 302a that regulate p53-effector genes.
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