Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study was carried out to assess the influence of saralasin (SAR), an angiotensin II-analogue, on peripheral and central angiotensin II-receptors by measurements of plasma renin activity (PRA) and arginine-vasopressin (AVP) release. Before and during i.v. infusion of 10 microgram/kg/min of SAR over a 30 minute period, blood samples were obtained from 15 recumbent hypertensive patients (7 renovascular, 8 essential) to determine hormone activities by radioimmunoassay. In 10 patients with a decrease of blood pressure following SAR, PRA increased significantly whereas AVP levels increased significantly in only 7 of these patients. In the remaining 5 patients without a fall of blood pressure, PRA and AVP remained virtually unchanged. The results indicate that an enhanced AVP release may be due to a hypotensive stimulus induced by SAR in angiotensinogenic hypertension. A direct influence of SAR on central receptors is unlikely under the conditions studied.
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PMID:Effect of saralasin on plasma renin activity and arginine-vasopressin in hypertensive man. 74 Jun 74

Arginine vasopressin in physiological concentrations potentiated the vascular effects of various vasoconstrictor agents. By using the isolated rat mesenteric artery preparation, the pressor effects of norepinephrine, angiotensin II, and potassium chloride were all significantly increased when vasopressin was added to the perfusion buffer. Cortisol and lithium both inhibited the potentiating effect of vasopressin but had no effect on the control pressor response to norepinephrine. When the vascular effects of norepinephrine were first blocked with indomethacin and then restored by the addition of prostaglandin E2, the potentiation by vasopressin was almost completely prevented. This suggests that vasopressin may be acting by stimulating prostaglandin biosynthesis. Cortisol and lithium may exert their inhibitory effects by preventing the activation of prostaglandin synthesis by vasopressin. These findings may be of clinical significance because the phenomena occur well within the range of vasopressin levels found in human plasma.
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PMID:Changes of vascular reactivity induced by low vasopressin concentrations: interactions with cortisol and lithium and possible involvement of prostaglandins. 74 21

The effect of isoproterenol (6 microgram/kg sc) on drinking, urine flow, and vasopressin secretion was examined in a group of trained dogs with chronically implanted third ventricular cannulae. Isoproterenol stimulated drinking in association with a reduction in urine flow and an increase in urine to plasma osmolality ratio. Plasma renin activity increased from 3.1 +/- 0.8 to 13.0 +/- 2.7 ng/ml/3 h and plasma vasopressin concentration increased from 11.3 +/- 1.3 to 40.3 +/- 12.5 pg/ml. The effect of isoproterenol was reexamined during an intracerebroventricular infusion of the angiotensin II antagonist, saralasin (0.02 microgram/kg/min). This treatment did not affect the isoproterenol-induced increase in plasma renin activity, but inhibited the drinking, antidiuresis, and increase in plasma vasopressin concentration. These data indicate that the effects of isoproterenol on drinking, urine flow, and vasopressin secretion are mediated via the renin-angiotensin system.
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PMID:Evidence that the effects of isoproterenol on water intake and vasopressin secretion are mediated by angiotensin. 74 84

1. In hepatocytes from starved rats, vasopressin, angiotensin (angiotensin II) and oxytocin stimulated gluconeogenesis from lactate by 25--50%; minimal effective concentrations were about 0.02pM, 1 nM and 0.2 nM respectively. 2. Vasopressin and angiotensin also stimulated gluconeogenesis from alanine, pyruvate, serine and glycerol. EGTA decreased gluconeogenesis from these substrates. 3. Hormonal stimulation of gluconeogenesis from lactate was abolished in the absence of extracellular Ca2+. 4. Insulin did not prevent stimulation of gluconeogenesis by vasopressin or angiotensin. 5. The potency of the stimulatory effects of vasopressin and angiotensin on hepatic gluconeogenesis suggests they are operative in vivo. Also, the data suggest that Ca2+ plays a role in the stimulation by these hormones.
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PMID:Stimulation by vasopressin, angiotensin and oxytocin of gluconeogenesis in hepatocyte suspensions. 74 59

Sodium excretion is correlated with kallikrein excretion in man, rabbits and rats on a free sodium and water intake, but not on a constant sodium or constant water intake. The correlation also exists during arterial infusion of angiotensin II, substance P and various vasodilators. During sodium depletion, the stimulation of the renin-angiotensin system causes increased drinking in rats and rabbits. The high angiotensin levels would stimulate kallikrein excretion. The excretion of water and dilution of urine are facilitated by the renal kallikrein-kinin system, even when antidiuretic hormone is high. This negative correlation between urinary osmolality and kallikrein excretion exists during arterial infusion of angiotensin or substance P and various vasodilators. During renal artery constriction, the kallikrein release per minute decreases, but over successive 10-minute periods, the kallikrein concentration in urine rises. This rise is correlated with some recovery in the clearance of rho-aminohippurate and inulin. Since kallikrein is released into renal lymph during saline infusion at a rate that correlates with its release into the urine, it is suggested that the renal kallikrein-kinin system protects the renal vasculature against the constricting action of the renin-angiotensin system. The decreased release of kallikrein (via the lymphatics into the circulation) during renal artery constriction, or decreased renal compliance, would potentiate the hypertensive effect of these procedures which cause increased renin release.
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PMID:The renal kallikrein-kinin system and the regulation of salt and water excretion. 76 62

1. Glycogen phosphorylase (a form, in rapidly freeze-clamped samples) and glucose release were measured in the perfused liver, in response to a range of concentrations of adrenaline, [8-arginine]vasopressin (anti-diuretic hormone) and angiotensin II. 2. All three hormones increased phosphorylase a activity by about 10 mumol/min per g of fresh liver, which was more than sufficient to explain concomitant glucose release (1-2mumol/min per g). 3. Minimally effective concentrations which activated phosphorylase were: adrenaline, 10nM (2ng/ml); vasopressin, 40pM (40pg/ml, 15 muunits/ml); angiotensin II, 60pM (60pg/ml). 4. Glycogen synthase activity was inhibited by adrenaline and vasopressin but not significantly by angiotensin II. 5. Vasoconstriction observed with adrenaline and angiotensin II (but not vasopressin) might explain part of the activation of phosphorylase, since equivalent vasoconstriction (in separate perfusions) activated phosphorylase, did not stimulate glucose output or inhibit synthase. 6. The potency of these effects suggests that all three hormones can stimulate hepatic glycogen degradation in vivo (by direct hepatic action). It is proposed that hormones, and ischaemia, stimulate glycogen degradation to provide glucose phosphates for disposal within the liver cell, as well as for release as free gluose.
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PMID:Glycogen phosphorylase, glucose output and vasoconstriction in the perfused rat liver. Concentration-dependence of actions of adrenaline, vasopressin and angiotensin II. 82 89

During the onset of malignant hypertension (MH) in rats treated with deoxycorticosterone trimethylacetate (DOC), plasma arginine vasopressin (AVP) concentrations increase tenfold as a consequence of hypovolemia and hyperosmolality. In benign hypertensive (BH) rats, plasma AVP is increased threefold in comparison with control animals. Plasma renin is markedly suppressed in both BH and MH animals. In MH rats, biologically active AVP antiserum lowers blood pressure (BP) transiently to normal or subnormal levels; in BH rats, a small BP-lowering effect of the AVP antiserum is seen. (Biologically active angiotensin II antiserum does not lower BP in MH rats.) The relationship between the height of BP and plasma AVP concentration in DOC hypertensive rats indicates, when compared with that relationship in diabetes insipidus rats infused with AVP, a marked enhancement of the vasopressor effect of AVP. These findings and the earlier observation of vasopressin-induced vascular damage by Byrom (F. B. Byrom, The Hypertensive Vascular Crisis. London: Heinemann, 1969) strongly suggest that ADH is involved as a vasopressor hormone in the pathogenesis of malignant DOC hypertension.
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PMID:Vasopressor role of ADH in the pathogenesis of malignant DOC hypertension. 84 73

Intravenous infusions of [Sar1-Ala8]angiotensin II, acute hypophysectomy, and acute intestinal denervation were carried out in 15 pentobarbital-anesthetized cats. Infusion of the angiotensin II antagonist caused only a small increase in superior mesenteric arterial conductance and a small decrease in arterial pressure in intact animals, but the changes were subypophysectomy alone caused only a small intestinal vasodilatation and little change in arterial pressure. However, the responses to hypophysectomy were much larger when the gland was removed during a prolonged infusion of the angiotensin II antagonist. Intestinal denervation caused only minor changes in mesenteric conductance and arterial pressure, and the responses to [Sar1-Ala8]angiotensin II and hypophysectomy were largely unaltered by the presence or absence of the intestinal innervation. The results suggest that the renin-angiotensin and vasopressin systems are reciprocal overlapping mechanisms that exert a significant vasoconstrictor influence on the intestinal resistance vessels in the anesthetized cat. In the absence of one control system, the other appears to compensate to maintain resistance.
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PMID:Vasopressin and angiotensin: reciprocal mechanisms controlling mesenteric conductance. 84 81

Various parameters of renal function were studied before, during, and after the infusion of physiological increments of angiotensin II directly into one renal artery of anesthetized dogs. During water diuresis and during antidiuresis induced with exogenous antidiuretic hormone (ADH), angiotensin II consistently reduced UNaV, UKV, and CPAH, and increased the filtration fraction in the infused kidney. Urinary osmolality was increased only in the presence of ADH, while during water diuresis angiotensin II had no apparent effect on urinary osmolality or flow rate. During saline diuresis, a mean increment of angiotensin II concentration of 14 pg/ml was sufficient to significantly reduce UNaV and urinary flow rate. Changes in CCr, CPAH, and filtration fraction did not correlate with changes in sodium excretion, and intracortical distribution of blood flow remained unaltered. These data support the hypothesis that normal circulating levels of angiogensin II play a direct renal role in the control of sodium, potassium, and water homeostasis, and that angiotensin II exerts a direct, stimulatory effect on tubular sodium reabsorption independent of changes in GFR, RPF, filtration fraction, or intracortical distribution of blood flow.
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PMID:Stimulation of renal sodium reabsorption by angiotensin II. 85 Nov 87

The brain isorenin angiotensin system has been implicated in the development of spontaneous hypertension by several investigators. The experiments reported here were designed to test the responsiveness of unanesthetized spontaneous hypertensive (SH) rats to intracerebroventricular angiotensin II injections compared to Wistar-Kyoto (WK) normotensive controls. The results indicate that there is no difference between SH and WK animals in drinking responses or antidiuretic hormone release to central angiotensin II injections; however, an increased pressor responsiveness to intraventricular angiotensin II in SH as compared to WK was observed. The results of intravenous infusions of pressor substances in these experiments and reports by other investigators suggest that the increased blood pressure effects to central angiotensin are due to three possible factors: 1) increased vascular responsiveness of SH to vasoconstrictor substances in general, 2) increased vascular sensitivity of SH rats to sympathetic outflow, and 3) decreased baroreceptor reflexes to acute increases in blood pressure. We suggest that the brain isorenin-angiotensin system may be involved in spontaneous hypertension by increased production of angiotensin II or by activation of a potentiated sympathetic system, but not by a generalized increased sensitivity of brain receptors to central angiotensin.
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PMID:Central angiotensin II-induced responses in spontaneously hypertensive rats. 85 Dec 5


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