UNIPROT:P01185 - FACTA Search

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Query: UNIPROT:P01185 (vasopressin)
23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Glomeruli contain receptors for many hormones. Binding of angiotensin II (ANG II) or antidiuretic hormone (ADH) to glomerular mesangial cells elicits a contractile response. Other hormones induce synthesis of cyclic nucleotides (cAMP, cGMP). Glomeruli also synthesize several prostaglandins, renin, and ANG II. Micropuncture studies in Munich-Wistar rats have examined the effects of vasoactive drugs and hormones on the filtration process. Several vasodilators increase renal plasma flow in the dog and rat, but GFR remains relatively unchanged due to an offsetting fall in the ultrafiltration coefficient (Kf). Vasoconstrictor substances such as ANG II and norepinephrine cause declines in renal plasma flow and Kf, but GFR remains constant due to an increase in the transcapillary hydraulic pressure gradient. Antidiuretic peptides and parathyroid hormone also reduce Kf. Glomerular mesangial cells may regulate Kf by contracting and reducing glomerular capillary surface area. ANG II and ADH directly stimulate mesangial cell contraction in vitro. Other hormones appear to cause contraction by inducing local ANG II synthesis. These hormonal pathways are implicated in the pathogenesis of altered glomerular function in diverse forms of renal injury.
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PMID:Hormonal modulation of glomerular function. 629 13

The role of vasopressin in the regulation of blood pressure during water deprivation was assessed in conscious dogs with two antagonists of the vasoconstrictor activity of vasopressin. In water-replete dogs, vasopressin blockade caused no significant changes in mean arterial pressure, heart rate, plasma renin activity (PRA), or plasma corticosteroid concentration. In the same dogs following 48-h water deprivation, vasopressin blockade increased heart rate from 85 +/- 6 to 134 +/- 15 beats/min (P less than 0.0001), increased cardiac output from 2.0 +/- 0.1 to 3.1 +/- 0.1 1/min (P less than 0.005), and decreased total peripheral resistance from 46.6 +/- 3.1 to 26.9 +/- 3.1 U (P less than 0.001). Plasma renin activity increased from 12.4 +/- 2.2 to 25.9 +/- 3.4 ng ANG I X ml-1 X 3 h-1 (P less than 0.0001) and plasma corticosteroid concentration increased from 3.2 +/- 0.7 to 4.9 +/- 1.2 micrograms/dl (P less than 0.05). Mean arterial pressure did not change significantly. When the same dogs were again deprived of water and pretreated with the beta-adrenoceptor antagonist propranolol, the heart rate and PRA responses to the antagonists were attenuated and mean arterial pressure decreased from 103 +/- 2 to 91 +/- 3 mmHg (P less than 0.001). These data demonstrate that vasopressin plays an important role in blood pressure regulation during water deprivation in conscious dogs.
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PMID:Role of vasopressin in blood pressure regulation in conscious water-deprived dogs. 633 15

The effect of leucine5-enkephalin (Leu-enkephalin) administered into the lateral (LV) or fourth (4V) cerebroventricle on angiotensin II (ANG II)-stimulated increase in blood pressure, plasma vasopressin concentration ([AVP]), and drinking behavior was determined in conscious rats. Leu-enkephalin (20, 50, or 100 micrograms) was injected into the LV (5 microliters) or 4V (2 microliters) less than or equal to 15 s before ANG II (50 or 500 ng, LV). LV and 4V administration of Leu-enkephalin (100 or 50 micrograms) significantly (P less than 0.05) delayed the drinking onset, decreased the number of animals drinking, and reduced the volume consumed (100 micrograms, 30 min) in response to ANG II (50 ng). ANG II-stimulated increases in plasma [AVP] and blood pressure were inhibited by 50 or 100 micrograms, respectively, of Leu-enkephalin administered into LV but not 4V. Decreased motor activity occurred after Leu-enkephalin (100 micrograms) administration into LV and 4V, whereas head shakes were more consistent after the former. Fast green dye administered into 4V did not reach anterior periaqueductal, third, or lateral cerebroventricular sites. Thus opioid peptide receptors inhibiting ANG II-stimulated drinking, vasopressin release, and pressor response are postulated to be in brain structures accessible from lateral or third cerebroventricles. Opiate receptors inhibitory to drinking are also reached from peri-4V sites.
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PMID:Cerebroventricular sites for enkephalin inhibition of the central actions of angiotensin. 634 May 33

The effects of 30-min intravenous infusions of 8-arginine vasopressin (AVP) and angiotensin-(1,8)-octapeptide (ANG II) to conscious dogs were studied by measurements of systolic (SABP), mean (MABP), and diastolic arterial blood pressures, central venous pressure (CVP), heart rate (HR), and plasma concentrations of vasopressin (pAVP). Infusion of AVP at six rates (0.4-12.8 ng X min-1 X kg-1) raised mean pAVP by 5-490 pg/ml and increased CVP by 2-10 cmH2O. HR decreased and arterial pressures increased with infusion rates of 1.6-12.8 ng X min-1 X kg-1. However, the increase in SABP was only transient. ANG II increased all arterial pressures; however, it barely changed CVP and did not change HR or pAVP. It is concluded that 1) AVP can elevate MABP without changes in SABP, 2) the effects of AVP on arterial pressures are buffered within 5-15 min, 3) CVP can be increased by doses of AVP that do not affect arterial pressures, and 4) the pressor activity is independent of the presence of ANG II. The results confirm that the cardiovascular response to vasopressin is qualitatively different from that elicited by ANG II.
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PMID:Effects on intravascular pressures of vasopressin and angiotensin II in dogs. 636 39

To investigate changes in plasma volume (PV) and osmolality as stimuli for plasma vasopressin (PVP) suppression and diuresis, seven normal healthy men (22-48 yr) were immersed to the neck for 4 h in a sitting position in tap water (34.5 degrees C) after overnight food and fluid restriction. Mean +/- SE urine volume was 823 +/- 123 ml/4 h; fluid intake was 400 ml/4 h, and mean negative water balance was 944 ml/4 h. Urinary sodium excretion increased from 0.77 to 1.25 mosmol/min (P less than 0.05) and UNaV from 0.14 to 0.37 meq/min (P less than 0.05). During immersion, PV (T-1824) increased by 8.8% (P less than 0.05) during the first 30 min and declined linearly thereafter. Mean +/- SD serum osmolality (294 +/- 1.2 mosmol/kg H2O) and sodium (143.2 +/- 0.4 meq/l) were constant throughout immersion; PVP (2.3 +/- 0.5 pg/ml) and plasma renin activity [0.3 +/- 0.2 ng ANG I/(ml X h]) were not significantly changed. Thus, the composition of the fluid entering the vascular space maintained constant serum osmolality and PVP throughout immersion. These findings do not support the hypothesis that acute expansion of central volume and PV cause suppression of PVP. The results suggest a mechanism other than or in addition to PVP suppression as a contributory cause of the immersion diuresis.
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PMID:Hypervolemia and plasma vasopressin response during water immersion in men. 636 63

The most primitive components of the RAS appeared early in the phylogenetic history of vertebrate animals. It is probable that renin granules were present in the kidneys of ancestral chordates before divergence in the evolution of actinopterygian fish and tetrapods occurred. Granulated juxtaglomerular cells similar to the renin-containing cells of the mammalian nephron are found in most extant vertebrate species although not in agnathan and elasmobranch fish. A macula densa occurs in amphibians, birds and mammals; and an extraglomerular mesangium, only in birds and mammals. Renin-like activity and angiotensin-like pressor material have been demonstrated in all classes of vertebrates. The amino acid sequences of native ANG I have been determined for representative species of teleost fish, amphibian, reptile and bird. These peptides differ from mammalian angiotensins at positions 1, 5 and 9. The RAS appears to be involved in osmoregulation, ionoregulation and the control of blood circulation. Prolonged hypovolemic hypotension or sodium depletion increases renin levels. Angiotensins elicit drinking and stimulate transepithelial ion transport. However, direct steroidogenic and antidiuretic hormone-releasing activities, which would promote mineral and fluid conservation, have not been demonstrated unambiguously in nonmammalian vertebrates. ANG II raises blood pressure by direct vasoconstrictor action on arteriolar muscles in some animals, but perhaps more generally by acting on the nervous system and adrenal paraneurons. In birds the hormone also has a hypotensive effect. ANG II stimulates the SNS in agnathans, elasmobranchs, teleosts, amphibians, reptiles, birds and mammals. Thus, modulation of sympathetic activity may be one of the most primitive and conservative functions of the RAS. For this reason, nonmammalian vertebrates are valuable models for studying the neurogenic actions of angiotensin II relevant to hypertensive disease.
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PMID:The renin-angiotensin system in nonmammalian vertebrates. 636 15

The anteroventral third ventricle (AV3V) region was shown to be a site of central integration of sympathetic pressor pathways and central pressor and vasopressin (VP) release by angiotensin II (ANG II). Since the AV3V area seems to have an important role in the regulation of the three major pressor systems, we investigated the role of the AV3V in cardiovascular recovery after hemorrhage, a known stimulus for sympathetic, ANG II, and VP release. Conscious AV3V-lesioned (n = 19) and sham-operated rats (n = 14) underwent bleeding (40% of blood volume) through an arterial line. Mean blood pressure, heart rate, and plasma ANG II, VP, and catecholamines were monitored over 24 h. The exact site of lesion was determined by microscopic examination. The mean blood pressure and heart rate of both groups of rats were not different before or after hemorrhage. Plasma catecholamines, ANG II, and VP responses were also the same as were hematocrit and water consumption 24 h after the bleeding. Despite the lack of difference between control and lesioned animals with regard to cardiovascular, humoral, and neuroendocrine responses to hypovolemia, the AV3V-lesioned rats had a significantly higher early mortality rate. These data indicate that the AV3V may be an important region in recuperation and survival after hemorrhagic shock, but through mechanisms unrelated to activation of VP, renin-ANG II, or the sympathetic nervous system.
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PMID:Anteroventral hypothalamus and hemorrhagic shock: cardiovascular and neuroendocrine responses. 637 15

Previous studies have shown that the inhibition of renin secretion by vasopressin (AVP) in conscious dogs is related to vasoconstrictor activity and may be a reflex response mediated by the renal nerves. The aim of the present experiments was to determine whether the suppression of plasma renin activity (PRA) by AVP is blocked by renal denervation. AVP and, for comparison, angiotensin II (ANG II) were infused intravenously for 45 min in seven conscious dogs before and after bilateral renal denervation. Before denervation, AVP infusion at 0.2 and 1.0 ng X kg-1 X min-1 suppressed PRA from 7.4 +/- 1.1 to 4.7 +/- 1.0 (P less than 0.01) and from 7.9 +/- 1.8 to 3.8 +/- 0.8 ng X ml-1 X 3 h-1 (P less than 0.01), respectively. ANG II infusion at 5.0 and 10.0 ng X kg-1 X min-1 decreased PRA from 7.5 +/- 2.3 to 2.5 +/- 0.7 (P less than 0.01) and from 6.0 +/- 1.1 to 1.8 +/- 0.4 ng X ml-1 X 3 h-1 (P less than 0.01), respectively. One to three weeks following renal denervation, PRA had decreased from 6.7 +/- 1.3 to 2.9 +/- 0.5 ng X ml-1 X 3 h-1 (P less than 0.01), and renal norepinephrine was undetectable. After denervation, neither AVP infusion at 0.2 (3.0 +/- 0.5 to 2.4 +/- 0.4 ng X ml-1 X 3 h-1) nor 1.0 ng X kg-1 X min-1 (3.1 +/- 0.8 to 2.8 +/- 1.0 ng X ml-1 X 3 h-1) suppressed PRA.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of renal denervation on the suppression of renin secretion by vasopressin in conscious dogs. 639 Dec 5

Arginine vasopressin (AVP) and angiotensin II (ANG II) reduce the glomerular filtration rate and ultrafiltration coefficient. Vasodilatory prostaglandins (PG) antagonize these effects. AVP and ANG II also cause mesangial cell contraction. Therefore, possible PG stimulation by these peptides and two vasopressin analogues was studied in cultured rat glomerular mesangial cells. The effect of altered calcium availability on PG production was also studied. Glomeruli from 75-100-g Sprague-Dawley rats were cultured in supplemented nutrient media for 28 d and experiments were performed on the first passage. Mesangial cell morphology was confirmed by electron microscopy. Cells produced PGE2 much greater than PGF2 alpha greater than 6-keto-PGF1 alpha greater than thromboxane B2 when incubated with the divalent cation ionophore, A23187, or arachidonic acid (C20:4). ANG II and AVP selectively stimulated PGE2 at threshold concentrations of 10 nM ANG II and 100 pM of AVP. The effects of the antidiuretic analogue 1-desamino-8-D-arginine vasopressin (dDAVP) and the antipressor analogue [1-(beta-mercapto-beta beta-cyclopentamethylene propionic acid)-4-valine, 8-D-arginine]-vasopressin (d[CH2]5VDAVP), were studied. Neither compound stimulated PGE2 and preincubation with d(CH2)5VDAVP abolished, and dDAVP blunted, AVP-enhanced PGE2 production. Incubation in verapamil, nifedipine, or zero calcium media blocked peptide-stimulated PGE2 production. Increasing extracellular calcium or adding A23187 increased PGE2 synthesis. Selective stimulation of PGE2 by ANG II or AVP in mesangial cells suggests a hormone-sensitive phospholipase and a coupled cyclooxygenase capable of synthesizing only PGE2. Since neither vasopressin analogue stimulated PGE2, but both blocked AVP-enhanced PGE2 production, we conclude that these cells respond to the pressor activity of AVP. This is a calcium-dependent process. Selective stimulation of PGE2 by ANG II and AVP may modulate their contractile effects on the glomerulus.
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PMID:Prostaglandin synthesis by rat glomerular mesangial cells in culture. Effects of angiotensin II and arginine vasopressin. 640 23

Renal cortical prostaglandin synthesis, particularly by arterioles and glomeruli, is important to preserve renal blood flow (RBF) and glomerular filtration rate (GFR). Glomeruli and arterioles synthesize not only the vasodilatory prostaglandins PGE2 and PGI2, but also the vasoconstrictor, thromboxane A2. The primary renal cortical actions of these prostaglandins are renal vasodilatation and maintenance of GFR (PGE2 and PGI2) or renal vasoconstriction and reduction of GFR (thromboxane A2). Vasodilatory renal prostaglandins are relatively unimportant under normal circumstances but play a modulatory role after ischemia or in the presence of increased concentrations of vasoconstrictor substances such as angiotensin II (ANG II), vasopressin or norepinephrine. ANG II and vasopressin stimulate the synthesis of PGE2 in rat glomerular epithelial and mesangial cells maintained in cell culture. These stimulatory actions of constrictor peptides are dependent upon calcium entry into the cells since removal of extracellular calcium or co-incubation with verapamil or nifedipine block the prostaglandin stimulatory capacity of ANG II or vasopressin. In vivo indomethacin potentiates the actions of ANG II on the kidney, particularly the reduction of RBF and GFR. Isolated rat glomeruli contract in response to ANG II and this contractile effect, which reflects reduction in glomerular filtration surface area, can be potentiated by cyclooxygenase blockade. Conversely, arachidonic acid reduces the glomerular contractile effect of ANG II. The importance of renal prostaglandins in support of RBF and GFR has been studied in dogs after chronic bile duct ligation (CBDL). CBDL dogs have significant increase in renal PGE2 and PGI2 which maintain RBF and GFR since cyclo-oxygenase inhibition resulted in a 50% decrease in both RBF and GFR. Indomethacin, ibuprofen, naproxen, and sulindac sulfide had comparable effects. The pro-drug, sulindac sulfoxide, was tested in normal volunteers and found to spare renal prostaglandin synthesis whereas indomethacin reduced renal synthesis of PGE2 and PGF2 alpha by more than 50%. In vitro, sulindac sulfide is a potent inhibitor of renal prostaglandin synthesis by kidney cells in culture. It is, therefore, concluded that renal prostaglandins play an important vasoregulatory role. Furthermore, sulindac sulfoxide may spare renal cyclo-oxygenase and thereby preserve renal function.
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PMID:Mechanisms of the nephrotoxicity of non-steroidal anti-inflammatory drugs. 659 99

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