Glomerular mesangial cells structurally support the tufts. Blood enters the capillaries of the glomerulus by a single arteriole called an afferent arteriole and leaves by an efferent arteriole. The capillaries consist of a tube lined by endothelial cells with a central lumen. The gaps between these endothelial cells are called fenestrae.
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The rest passes into an efferent arteriole. The diameter of the efferent arteriole is smaller than that of the afferent, and this difference increases the hydrostatic pressure in the glomerulus.
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Arteriole diameters decrease with age and with exposure to air pollution.
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Additionally, vasopressin selectively contracts efferent arterioles probably through the V1R, but not the afferent arteriole.
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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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Spider angiomas form due to failure of the sphincteric muscle surrounding a cutaneous arteriole. The central red dot is the dilated arteriole and the red "spider legs" are small capillaries carrying away the freely flowing blood. If momentary pressure is applied, it is possible to see the emptied capillaries refilling from the center. No other angiomas show this phenomenon.
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Decreased diameter of Arteriole. Any pathology which constricts blood flow, such as stenosis, will increase total peripheral resistance and lead to hypertension.
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The juxtaglomerular cells in the afferent arteriole constrict, and juxtaglomerular cells in both the afferent and efferent arteriole decrease their renin secretion. These actions function to lower GFR. Further increase in sodium concentration leads to the release of nitric oxide, a vasodilating substance, to prevent excessive vasoconstriction. In the opposite case, juxtaglomerular cells are stimulated to release more renin, which stimulates the renin–angiotensin system, producing angiotensin I which is converted by Angio- Tensin Converting Enzyme (ACE) to angiotensin II. Angiotensin II then causes preferential constriction of the efferent arteriole of the glomerulus and increases the GFR.
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Arteriovenous nicking, also known as AV nicking, is the phenomenon where, on examination of the eye, a small artery (arteriole) is seen crossing a small vein (venule), which results in the compression of the vein with bulging on either side of the crossing. This is most commonly seen in eye disease caused by high blood pressure (hypertensive retinopathy). It is thought that, since the arteriole and venule share a common sheath, the arteriole's thicker walls push against those of the venule forcing the venule to collapse. This makes the venule form an hourglass shape around the arteriole.
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The JGA is located between the thick ascending limb and the afferent arteriole. It contains three components: the macula densa, juxtaglomerular cells, and extraglomerular mesangial cells.
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Arteriolosclerosis is the term specifically used for the hardening of arteriole walls. This can be due to decreased elastic production from fibrinogen, associated with ageing, or hypertension or pathological conditions such as atherosclerosis.
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The walls of the afferent arteriole contain specialized smooth muscle cells that synthesize renin. These juxtaglomerular cells play a major role in the renin–angiotensin system, which helps regulate blood volume and pressure.
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In the spine, similar fibres join the intervertebral disc to the adjacent vertebrae. Each fibre is accompanied by an arteriole and one or more nerve fibres. Scottish anatomist William Sharpey described them in 1846.
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Acetylcholine is released, leads to an increased extracellular calcium, which causes extracellular hyperpolarization followed by dilation of the arteriole. The redness leads to the flare response of the axon reflex.Tuma, Ronald. Microcirculation. Academic Press, 2011, p. 297.
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This blood leaves the glomerulus via the efferent arteriole, which supplies the peritubular capillaries. The higher osmolarity of the blood in the peritubular capillaries creates an osmotic pressure which causes the uptake of water. Other ions can be taken up by the peritubular capillaries via solvent drag. Water is also driven into the peritubular capillaries due to the higher fluid pressure of the interstitium, driven by reabsorption of fluid and electrolytes via active transport, and the low fluid pressure of blood entering the peritubular capillaries due to the narrowness of the efferent arteriole.
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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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In hypertension only the afferent arteriole is affected, while in diabetes mellitus, both the afferent and efferent arteriole are affected. ;Cause Lesions reflect leakage of plasma components across vascular endothelium and excessive extracellular matrix production by smooth muscle cells, usually secondary to hypertension. Hyaline arteriolosclerosis is a major morphologic characteristic of benign nephrosclerosis, in which the arteriolar narrowing causes diffuse impairment of renal blood supply, with loss of nephrons. The narrowing of the lumen can decrease renal blood flow and hence glomerular filtration rate leading to increased renin secretion and a perpetuating cycle with increasing blood pressure and decreasing kidney function.
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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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This results in a smaller capillary hydrostatic pressure, which causes an increased absorption of sodium ions into the vasa recta at the proximal tubule. Hence, a decrease in blood pressure results in less sodium chloride present at the distal tubule, where the macula densa is located. The macula densa senses this drop in salt concentration and responds through two mechanisms, both of which are mediated by prostaglandin release. First, prostaglandins preferentially vasodilate the renal afferent arteriole, decreasing afferent arteriole resistance and, thus, offsetting the decrease in glomerular hydrostatic pressure caused by the drop in blood pressure.
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The viscoelastic pads decrease ischemia, pain, and discomfort for patients undergoing MRI studies. His MRI research led to improved quality of the MRI imaging studies to improve patient care, He has also studied the effect of nicotine on bone arteriole blood flow.
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The juxtaglomerular apparatus is part of the kidney nephron, next to the glomerulus. It is found between afferent arteriole and the distal convoluted tubule of the same nephron. This location is critical to its function in regulating renal blood flow and glomerular filtration rate.
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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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Vasodilation of the afferent arteriole, which results in increased glomerular filtration pressure and tubular fluid flow, occurs when MD cells detect a chloride concentration that is below a target value. A higher fluid flow rate in the TAL allows less time for dilution of the tubular fluid so that MD chloride concentration increases. Glomerular flow is decreased if the chloride concentration is above the target value. Constricting the smooth muscle cells in the afferent arteriole, results in a reduced concentration of chloride at the MD. TGF stabilizes the fluid and solute delivery into the distal portion of the loop of Henle and maintain the rate of filtration near its ideal value using these mechanisms.
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Vasopressin antagonists :Tolvaptan showed to have no benefit. It is also a very costly drug. Adenosine antagonists :Adenosine is responsible for constriction of afferent arteriole and reduction in GFR. It was found that an adenosine A1-receptor antagonist called KW-3902 was able to improve kidney function in CRS patients.
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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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Dieulafoy's lesion (or Dieulofoy lesion) is a medical condition characterized by a large tortuous arteriole most commonly in the stomach wall (submucosal) that erodes and bleeds. It can present in any part of the gastrointestinal tract. It can cause gastric hemorrhage but is relatively uncommon. It is thought to cause less than 5% of all gastrointestinal bleeds in adults.
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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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Schweigger-Seidel sheath is a phagocytic sleeve that is part of a sheathed arteriole of the spleen, and is sometimes referred to as a splenic ellipsoid. It is a spindle-shaped thickening in the walls of the second part of the arterial branches forming the penicilli in the spleen. It is named after German physiologist Franz Schweigger-Seidel (1834-1871).
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The response involves pupil dilation, release of endorphins, increased heart and respiration rates, cessation of digestive processes, secretion of adrenaline, arteriole dilation, and constriction of veins. This high level of arousal is often unnecessary to adequately cope with micro- stressors and daily hassles; yet, this is the response pattern seen in humans, which often leads to health issues commonly associated with high levels of stress.
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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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Demachy died of arteriole sclerosis in Hennequeville, Normandy, on 29 December 1936. He was buried two days later in the family tomb at Père Lachaise Cemetery in Paris. Just before his death he destroyed most of his sketches and gave any remaining photographs to the Royal Photographic Society and the Photo-Club de Paris. The Banque Demachy still exists today but is no longer connected to the original family.
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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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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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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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"Onion-skin" renal arteriole This is a type of arteriolosclerosis involving a narrowed lumen. The term "onion-skin" is sometimes used to describe this form of blood vessel with thickened concentric smooth muscle cell layer and thickened, duplicated basement membrane. In malignant hypertension these hyperplastic changes are often accompanied by fibrinoid necrosis of the arterial intima and media. These changes are most prominent in the kidney and can lead to ischemia and acute kidney failure.
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Glomus tumors were first described by Hoyer in 1877 while the first complete clinical description was given by Masson in 1924. Histologically, glomus tumors are made up of an afferent arteriole, anastomotic vessel, and collecting venule. Glomus tumors are modified smooth muscle cells that control the thermoregulatory function of dermal glomus bodies. As stated above, these lesions should not be confused with paragangliomas, which were formerly also called glomus tumors in now-antiquated clinical usage.
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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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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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It may be involved in breast cancer, and its protein signaling is, it is presumed, a molecular switch that governs adipogenesis. Gain-of-function of Wnt10b in mouse hearts has shown to improve cardiac tissue repair after myocardial injury, by promoting coronary vessel formation and attenuating pathological fibrosis.Paik DT, Rai M, Ryzhov S, Sanders LN, Aisagbonhi O, Funke MJ, Feoktistov I, Hatzopoulos AK. Wnt10b gain-of-function improves cardiac repair by arteriole formation and attenuation of fibrosis. Circ Res.
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The syndrome occurs predominantly in middle-aged women with poorly controlled hypertension in the form of skin ulcers on the anterolateral aspect of the lower legs. The lesions initially appear as small, painful blisters which may or may not be associated with trauma. The pathophysiology of the Martorell ulcer is assumed to be related to hypertension-induced arteriole changes in the dermis. The pain is often disproportionate, and the symptoms are not relieved by rest or elevation.
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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 reason for this lies in the mechanism of filtration of BUN and creatinine. Renal Plasma Flow (RPF) is decreased due to hypoperfusion which results in a proportional decrease in GFR. In turn, the decreased flow and pressure to the kidney will be sensed by baroreceptors in the Juxtaglomerular (JG) Cells of the afferent arteriole. If the decrease in blood pressure is systemic (rather than occlusion of the renal artery) baroreceptors in the carotid sinus and aortic arch will be stimulated.
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The glomerulus is the network known as a tuft, of filtering capillaries located at the vascular pole of the renal corpuscle in Bowman's capsule. Each glomerulus receives its blood supply from an afferent arteriole of the renal circulation. The glomerular blood pressure provides the driving force for water and solutes to be filtered out of the blood plasma, and into the interior of Bowman's capsule, called Bowman's space. Only about a fifth of the plasma is filtered in the glomerulus.
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In vertebrates, potentially painful stimuli typically produce vegetative modifications such as tachycardia, pupil dilation, defecation, arteriole blood gases, fluid and electrolyte imbalance, and changes in blood flow, respiratory patterns, and endocrine. The crayfish Procambarus clarkii At the cellular level, injury or wounding of invertebrates leads to the directed migration and accumulation of haematocytes (defence cells) and neuronal plasticity, much the same as the responses of human patients undergoing surgery or after injury.Clatworthy, A.L., (1996). A simple systems approach to neural-immune communication.
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The epidermis primarily consists of keratinocytes (proliferating basal and differentiated suprabasal), which comprise 90% of its cells, but also contains melanocytes, Langerhans cells, Merkel cells, and inflammatory cells. Epidermal thickenings called Rete ridges (or rete pegs) extend downward between dermal papillae.TheFreeDictionary > rete ridge Citing: The American Heritage Medical Dictionary Copyright 2007, 2004 Blood capillaries are found beneath the epidermis, and are linked to an arteriole and a venule. The epidermis itself has no blood supply and is nourished almost exclusively by diffused oxygen from the surrounding air.
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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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Diuretics act by lowering water and sodium levels; this causes more reabsorption of lithium in the proximal tubules so that the removal of lithium from the body is less, leading to increased blood levels of lithium. ACE inhibitors have also been shown in a retrospective case-control study to increase lithium concentrations. This is likely due to constriction of the afferent arteriole of the glomerulus, resulting in decreased glomerular filtration rate and clearance. Another possible mechanism is that ACE inhibitors can lead to a decrease in sodium and water.
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Ramipril 1.25-mg oral capsule, letter codes and icons may differ ACE inhibitors inhibit the actions of angiotensin converting enzyme (ACE), thereby lowering the production of angiotensin II and decreasing the breakdown of bradykinin. The decrease in angiotensin II results in relaxation of arteriole smooth muscle leading to a decrease in total peripheral resistance, reducing blood pressure as the blood is pumped through widened vessels. Its effect on bradykinin is responsible for the dry cough side effect. Ramipril, a prodrug or precursor drug, is converted to the active metabolite ramiprilat by carboxylesterase 1.
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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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The blood hammer phenomenon is a sudden increase of the upstream blood pressure in a blood vessel (especially artery or arteriole) when the bloodstream is abruptly blocked by vessel obstruction. The term "blood-hammer" was introduced in cerebral hemodynamics by analogy with the hydraulic expression "water hammer", already used in vascular physiology to designate an arterial pulse variety, the "water-hammer pulse". Complete understanding of the relationship between mechanical parameters in vascular occlusions is a critical issue, which can play an important role in the future diagnosis, understanding and treatment of vascular diseases.
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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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Inulin is uniquely treated by nephrons in that it is completely filtered at the glomerulus but neither secreted nor reabsorbed by the tubules. This property of inulin allows the clearance of inulin to be used clinically as a highly accurate measure of glomerular filtration rate (GFR) — the rate of plasma from the afferent arteriole that is filtered into Bowman's capsule measured in ml/min. It is informative to contrast the properties of inulin with those of para-aminohippuric acid (PAH). PAH is partially filtered from plasma at the glomerulus and not reabsorbed by the tubules, in a manner identical to inulin.
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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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Activation of aortic smooth muscle doesn't significantly alter the lumenal diameter but serves to increase the viscoelasticity of the vascular wall. In the digestive tract, smooth muscle contracts in a rhythmic peristaltic fashion, rhythmically forcing foodstuffs through the digestive tract as the result of phasic contraction. A non-contractile function is seen in specialized smooth muscle within the afferent arteriole of the juxtaglomerular apparatus, which secretes renin in response to osmotic and pressure changes, and also it is believed to secrete ATP in tubuloglomerular regulation of glomerular filtration rate. Renin in turn activates the renin–angiotensin system to regulate blood pressure.
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Each straight arteriole has a hairpin turn in the medulla and carries blood at a very slow rate – two factors crucial in the maintenance of countercurrent exchange that prevent washout of the concentration gradients established in the renal medulla. The maintenance of this concentration gradient is one of the components responsible for the kidney's ability to produce concentrated urine. On the descending portion of the vasa recta, sodium chloride and urea are reabsorbed into the blood, while water is secreted. On the ascending portion, sodium chloride and urea are secreted into the interstitium, while water is reabsorbed.
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Angiotension converting enzyme The pathogenesis of renovascular hypertension involves the narrowing of the arteries supplying the kidneys which causes a low perfusion pressure that is detected by the juxtaglomerular apparatus (via the macula densa cells, which act as baroreceptors; located on the afferent arteriole wall). This leads to renin secretion that causes the angiotensinogen conversion to angiotensin I. Angiotensin I then proceeds to the lung where it is converted to angiotensin II via angiotensin converting enzyme (ACE). In most people fibromuscular dysplasia or atherosclerosis is the reason for the occlusion of a renal artery which ultimately leads to this condition.
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Dieulafoy lesions are characterized by a single abnormally large blood vessel (arteriole) beneath the gastrointestinal mucosa (submucosa) that bleeds, in the absence of any ulcer, erosion, or other abnormality in the mucosa. The size of these blood vessels varies from 1–5 mm (more than 10 times the normal diameter of mucosal capillaries). Pulsation from the enlarged vessels leads to focal pressure that causes thinning of the mucosa at that location, leading to exposure of the vessel and subsequent hemorrhage. Approximately 75% of Dieulafoy's lesions occur in the upper part of the stomach within 6 cm of the gastroesophageal junction, most commonly in the lesser curvature.
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In the renal system, peritubular capillaries are tiny blood vessels, supplied by the efferent arteriole, that travel alongside nephrons allowing reabsorption and secretion between blood and the inner lumen of the nephron. Peritubular capillaries surround the cortical parts of the proximal and distal tubules, while the vasa recta go into the medulla to approach the loop of Henle. About one-fifth of the blood plasma is filtered as the blood passes through the glomerular capillaries; four-fifths continues into the peritubular capillaries. Ions and minerals that need to be saved in the body are reabsorbed into the peritubular capillaries through active transport, secondary active transport, or transcytosis.
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Extraglomerular mesangial cells (also known as Lacis cells, Polkissen cells, or Goormaghtigh cells) are light-staining pericytes in the kidney found outside the glomerulus, near the vascular pole. They resemble smooth muscle cells and play a role in renal autoregulation of blood flow to the kidney and regulation of systemic blood pressure through the renin–angiotensin system. Extraglomerular mesangial cells are part of the juxtaglomerular apparatus, along with the macula densa cells of the distal convoluted tubule and the juxtaglomerular cells of the afferent arteriole. The specific function of extraglomerular mesangial cells is not well understood, although it has been associated with the secretion of erythropoietin and secretion of renin.
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Schematic depicting how the RAAS works. Here, activation of the RAAS is initiated by a low perfusion pressure in the juxtaglomerular apparatus Macula densa cells sense changes in sodium chloride level, and will trigger an autoregulatory response to increase or decrease reabsorption of ions and water to the blood (as needed) in order to alter blood volume and return blood pressure to normal. A decrease in afferent arteriole diameter causes a decrease in the GFR (glomerular filtration rate), resulting in a decreased concentration of sodium and chloride ions in the filtrate and/or decreased filtrate flow rate. Reduced blood pressure means decreased venous pressure and, hence, a decreased peritubular capillary pressure.
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Thus, the TAL is an important segment of the TGF system, and its transport properties allow it to act as a key operator of the TGF system. A reduction of GFR occurs as a result of TGF when NaCl concentration at the sensor site is increased within the physiological range of approximately 10 to 60 mM. The TGF mechanism is a negative feedback loop in which the chloride ion concentration is sensed downstream in the nephron by the macula densa (MD), cells in the tubular wall near the end of TAL and the glomerulus. The muscle tension in the afferent arteriole is modified based on the difference between the sensed concentration and a target concentration.
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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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Indirect studies in animal models suggest that EETs have protective effects in strokes (i.e. cerbrovasular accidents). Thus, sEH inhibitors and sEH-Gene knockout have been shown to reduce the damage to brain that occurs in several different models of ischemic stroke; this protective effect appears due to a reduction in systemic blood pressure and maintenance of blood flow to ischemic areas of the brain by arteriole dilation as a presumed consequence of inhibiting the degradation of EETs (and/or other fatty acid epoxides). sEH-gene knockout mice were also protected from that brain damage that followed induced-subarachnoid hemorrhage; this protective effect appeared due to a reduction in cerebral edema which was also presumable due to the prolongation of EET half-lives.
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The oxygen stored is insufficient for aerobic consumption by all tissues, and differential distribution of blood oxygen store to the brain can allow less sensitive tissues to function anaerobically during a dive. Peripheral vasoconstriction largely excludes the skeletal muscles from perfusion during a dive, and use the oxygen stored locally in myoglobin, followed by anaerobic metabolism during a dive. When breathing again, the muscles are perfused and re-oxygenated, and there is a surge in arterial lactate for a short period until reoxygenation stabilises. The problem of how the arteries remain constricted in the presence of increasing tissue pH due to intracellular lactate was found to be avoided by the ability to constrict arteries leading to the organs, rather than arteriole constriction within the organs as occurs in terrestrial animals.
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The macula densa region of the kidney's juxtaglomerular apparatus is another modulator of blood osmolality. The macula densa responds to changes in osmotic pressure through changes in the rate of sodium ion (Na+) flow through the nephron. Decreased Na+ flow stimulates tubuloglomerular feedback to autoregulate, a signal (thought to be regulated by adenosine) sent to the nearby juxtaglomerular cells of the afferent arteriole, causing the juxtaglomerular cells to release the protease renin into circulation. Renin cleaves the zymogen angiotensinogen, always present in plasma as a result of constitutive production in the liver, into a second inactive form, angiotensin I, which is then converted to its active form, angiotensin II, by angiotensin converting enzyme (ACE), which is widely distributed in the small vessels of the body, but particularly concentrated in the pulmonary capillaries of the lungs.
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EPA- and DHA-rich) diet produced significant reductions in systolic blood pressure and increased peripheral arteriole blood flow and reactivity in patients at high to intermediate risk for cardiovascular events; an EPA/DHA- rich diet also reduced the risk while high serum levels of DHA and EPA were associated with a low risk of neovascular age-related macular degeneration. Since such diets lead to large increases in the serum and urine levels of EPAs, EEQs, and the dihydoxy metabolites of these epoxides but relatively little or no increases in EETs or lipoxygenase/cyclooxygenase-producing metabolites of arachidonic acid, DHA, and/or EEQs, it is suggested that the diet-induced increases in EPAs and/or EEQs are responsible for this beneficial effects. In direct contrast to the EETs which have stimulating effects in the following activities (see Epoxyeicosatrienoic acid#Cancer, EEQs (and EPAs) inhibit new blood vessel formation (i.e. angiogenesis), human tumor cell growth, and human tumor metastasis in animal models implanted with certain types of human cancer cells.
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