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

Recent evidence suggests that angiotensin II (ANG II) and vasopressin (AVP) act on the liver via specific receptors. We have examined the binding properties of these receptors in isolated rat hepatocytes and studied the regulation of the biological responses to ANG II and AVP during pregnancy in the rat. In contrast to [3H]ANG II, 125I-labeled-[Sar1-Ile8]ANG II was markedly resistant to degradation by isolated liver cells. Displacement and saturation experiments with this iodinated antagonist revealed the presence of a single class of binding sites [2 x 10(5) sites/cell, dissociation constant (KD) = 1.0 nM]. The potency of ANG II analogues to displace 125I-[Sar1-Ile8]-ANG II agrees closely with data reported for vascular smooth muscle cells. Isolated hepatocytes have approximately 8 x 10(4) [3H]AVP binding sites/cell (KD = 1.0 nM) based on saturation experiments. AVP analogues selectively displaced [3H]AVP, suggesting the presence of V1-AVP receptor subtype. The maximum response of [Sar1]ANG II-induced glycogenolysis in the cells was decreased during gestation, whereas the effective concentration producing 50% of maximum response (EC50) was significantly increased (0.15-0.28 nM) when compared with cells from nonpregnant animals. In pregnancy, receptors for 125I-[Sar1-Ile8]ANG II were not changed in affinity (KD) or in density (Bmax). The maximum response and EC50 of AVP on liver glycogenolysis were not significantly decreased during pregnancy, whereas an increased number of AVP binding sites (from 5.0 +/- 0.5 x 10(4) to 11.0 +/- 1.7 x 10(4)) with similar KD was observed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Regulation of ANG II and AVP receptors in isolated hepatocytes of pregnant rats. 233 59

Intracerebroventricular (ivt) angiotensin II (ANG II) at 0.4, 2, 10, and 50 ng.kg-1.min-1 increased arterial pressure in conscious sheep in a dose-related manner (26 mmHg, P less than 0.05, at 50 ng.kg-1.min-1). Total peripheral resistance (TPR) and right atrial pressure also increased. Heart rate, stroke volume, and cardiac output did not change. Pressor responses to ivt ANG II were not caused by leakage of ANG II into the periphery, because plasma concentrations of ANG II did not change from control (31 +/- 7 pg/ml) at the highest dose of ANG II infused. In contrast, intravenous (iv) ANG II, 10 and 50 ng.kg-1.min-1, increased arterial pressure 29 and 47 mmHg, respectively (P less than 0.05), and decreased heart rate. ANG II, 10 ng.kg-1.min-1 iv, increased plasma ANG II levels from 36 +/- 6 to 354 +/- 69 pg/ml (P less than 0.05). Intracarotid (ic) ANG II, 10 ng.kg-1.min-1, increased arterial pressure 31 mmHg (P less than 0.05) but did not alter heart rate. ANG II ivt caused a dose-related drinking response, with a positive correlation between the amount of water drunk during ivt ANG II infusion and the increase in arterial pressure. Infusions of ANG II at 50 ng.kg-1.min-1 ivt were associated with decreased plasma osmolality and potassium concentration and increased plasma vasopressin concentration.
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PMID:Hemodynamic and behavioral effects of angiotensin II in conscious sheep. 233

The microcirculatory effects of vasoactive peptides on arteriolar diameter were determined in the dorsal skin-fold preparation of conscious Syrian hamsters and related to arterial blood pressure (MABP). (5 Ile)-angiotensin II (ANG II), (8 Arg)-vasopressin (AVP), vasoactive intestinal polypeptide (VIP), atrial natriuretic factor (ANF), and substance P (SP) were administered intravenously as bolus injections in picomolar concentrations. The diameters of subcutaneous A3 arterioles (15-40 microns) at bifurcation sites were determined via a microscope video system and stored in a digital memory. When spontaneous rhythmic vasoconstrictions and dilations (vasomotion) were present, the diameter oscillations were analyzed by means of the Prony Spectral Line Estimator. ANG II caused sustained arteriolar contraction at increased MABP, but did neither induce nor modulate vasomotion. Both ANF and VIP slightly reduced MABP and had no effect on microcirculatory parameters. SP led to a significant dilation of subcutaneous arterioles in the hamster skin with concomitant drop in MABP, but did not influence arteriolar vasomotion. Physiological concentrations of AVP, as determined in the plasma by radioimmunoassay, caused a marked contraction of the arterioles and evoked a mild pressor response. In addition, AVP induced or greatly enhanced vasomotoric activity. This study therefore provides evidence that endogenous vasoactive peptides play an important role in regulation of skin peripheral resistance by altering arteriolar diameter in a tonic or even dynamic way.
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PMID:Regulatory role of vasoactive peptides in subcutaneous skin microcirculation of the hamster. 245 Aug 51

We have investigated the effect of infusions of arginine vasopressin on cardiac output and O2 uptake in the presence and in the absence of sinoaortic reflexes to better understand the mechanism of the exaggerated decrease in cardiac output elicited by vasopressin. Chronically instrumented dogs received, on separate days, 30-min infusions of vasopressin (0.2, 1, 5, 20, and 60 ng.kg-1.min-1), phenylephrine (1, 3, and 10 micrograms.kg-1.min-1), and angiotensin II (ANG II) (10, 20, and 50 ng.kg-1.min-1). These infusions all increased mean arterial pressure to a maximum of 63 +/- 8.2 mmHg during the highest phenylephrine infusion rate. Vasopressin reduced cardiac output (electromagnetic flowmeter) more than the other vasoconstrictors for equivalent increases in arterial pressure. Vasopressin also produced dose-dependent decreases in O2 uptake, measured by collection of expired air. Such decreases were not observed with the other two agents. On the contrary, ANG II and phenylephrine increased O2 uptake significantly when they decreased cardiac output the most. The decrease in O2 uptake induced by vasopressin was significantly correlated with the decrease in cardiac output. Pretreatment of the dogs with atropine prevented the decrease in O2 uptake and blunted the fall in cardiac output induced by vasopressin at a rate of 5 ng.kg-1.min-1. In dogs surgically deprived of sinoaortic receptors, vasopressin given at 1 and 5 ng.kg-1.min-1 failed to reduce O2 uptake and cardiac output significantly.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Vasopressin reduces oxygen uptake in intact dogs but not in sinoaortic-denervated dogs. 250 32

Atrial natriuretic factor (ANF) and angiotensin II (ANG II) have been demonstrated in close vicinity in forebrain areas involved in the central fluid and electrolyte regulation. Previous reports suggested an inhibitory effect of ANF on some of the central actions of ANG II, such as water intake and vasopressin release. In the present study in conscious, unrestrained, sodium-repleted rats we investigated the effects of intracerebroventricularly (i.c.v.) administered ANF (alpha r-APIII) on the central natriuretic action of ANG II. Urine was collected through a novel chronically implanted ureteral catheter. I.c.v. injections of ANG II (100 pg) produced a marked natriuresis of rapid onset without altering urinary volume or blood pressure. Pretreatment with ANF (100 pg, 1 ng, 100 ng i.c.v.) 5 min before ANG II dose-dependently antagonized the ANG II-induced natriuretic effect. The lowest dose caused approximately 50% reduction, the intermediate dose a complete abolition and the highest dose even a reversal of the ANG II-induced natriuretic effect to salt retention. Urinary volume and blood pressure were not altered by the combined treatment with ANG II and ANF. Our results support the idea of a functional antagonism between ANG II and ANF in the central fluid and electrolyte control.
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PMID:Centrally administered atrial natriuretic factor inhibits central angiotensin-induced natriuresis. 253 Oct 13

Hypotension stimulates the secretion of adrenocorticotropin (ACTH) and vasopressin (AVP) and increases plasma levels of angiotensin II (ANG II). Because AVP and ANG II increase ACTH secretion, the present experiments were performed to evaluate the role of these peptides in the increases in plasma ACTH and glucocorticoid concentrations produced by hypotension in conscious dogs. This was accomplished by determining whether administration of receptor antagonists to vasopressin, [1-(beta-mercapto-beta,beta-cyclopentamethylene propionic acid), 2-(O-methyl)tyrosine]Arg8-vasopressin, and ANG II (saralasin), reduced the ACTH and glucocorticoid responses to infusion of four doses of the vasodilator nitroprusside. Nitroprusside (NP) infusion produced dose-dependent decreases in mean arterial pressure. Larger decreases in arterial pressure were produced in dogs pretreated with the AVP antagonist or with both saralasin and the vasopressin antagonist. Left and right atrial pressures also fell with NP infusion, and larger decreases in atrial pressures were found in dogs pretreated with the AVP antagonist. Finally, NP infusion increased plasma glucocorticoid concentration and plasma ACTH concentration. Both the glucocorticoid and the ACTH responses to hypotension were reduced in dogs given the AVP antagonist and in dogs given both saralasin and the AVP antagonist, but there was no difference in the effect of AVP blockade alone vs. the effect of combined AVP and ANG II blockade. These data suggest that AVP, but not ANG II, is required for normal glucocorticoid and ACTH responses to hypotension. They also suggest that AVP is necessary for normal maintenance of arterial blood pressure and atrial pressures during NP infusion.
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PMID:Vasopressin and ANG II in the control of ACTH secretion and arterial and atrial pressures. 253 37

To assess angiotensin (ANG II) dependence of evolving neonatally induced coarctation hypertension (NICH) in inbred pups, we randomized sex-matched littermates to high-dose converting enzyme inhibitor (CEI: MK-421, 3 mg/kg) or placebo from the time of neonatal aortic banding (coarcted) vs. no banding (control). During phase 1 studies over 4 mo postbanding during ad libitum Na+ intake (Bagby and Fuchs, Hypertension Dallas in press). CEI failed to prevent evolution of proximal blood pressure (BP) excess or to impair renal function. Phase 2 studies examine, in the same pups, responses to low Na+ (LS) diet superimposed on chronic CEI at 4 mo, timed to allow development of BP increase in untreated NICH. The present report details metabolic handling and balances of Na+, K+, and fluid for 3 days before (normal Na+ intake) and daily for 11 days after initiation of LS diet, a companion paper describes BP, renin-angiotensin (RA), and renal functional responses. In no case did metabolic responses of coarcted pups to LS diet differ from those of controls, whether on CEI or placebo, whereas responses to LS diet and to CEI reveal positive findings of independent interest. LS diet induced expected renal and fecal Na+ conservation, no net effect on K+ balance, and, despite unexpected free-water diuresis, mild hyponatremia. Chronic CEI impaired maximal renal (but not fecal) Na+ conservation during LS diet, caused exaggerated free-water diuresis but no change in fluid balance, and thus, with the larger Na+ deficit, accounted for greater hyponatremia. CEI caused no net effect on K+ balance. Results indicate normal renal handling of fluid, Na+, and K+ in evolving NICH and provide no evidence for selective intrarenal RA activation or exaggerated ANG II dependence. Findings also suggest that, during LS diet, ANG II is 1) essential for maximum renal Na+ conservation and normal free-water handling, and 2) not essential for fecal Na+ and water conservation or for maintenance of normal water and K+ balances. Results are also compatible with a CEI-induced thirst stimulation and/or osmotic insensitivity and with functional vasopressin deficiency during LS diet.
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PMID:Chronic CEI alters effect of low Na+ diet in normal and coarcted pups. II. Na+ and H2O balance. 253 43

Potentiated adrenocorticotropin (ACTH) and cortisol responses occur after the second of two small hemorrhages (hems) spaced 24 h apart in the dog. To test whether increased responses of other hormones might be associated with this effect, we examined plasma renin activity (PRA), angiotensin II (ANG II), and vasopressin after paired 10% hem (H1 and H2) spaced 5 h apart in chronically prepared conscious dogs. Cortisol secretion increased after each hem, and the response to H2 was larger (P less than 0.05; H1 peak at 6.8 +/- 1.3 micrograms/min vs. H2 peak at 18.3 +/- 5.3 micrograms/min). ACTH did not change after H1 but increased after H2, and the H2 response was larger (P less than 0.01). Vasopressin increased after each hem, and the H2 response was larger (P less than 0.01). The time courses of ACTH and vasopressin responses were similar after H2 (significant increases by 8 min). PRA and ANG II increased by 4 min after each hem, and although the difference was small the early PRA and ANG II responses were greater after H2. Blood volume and hem volume did not differ between hems. Hemodynamic responses to the hems were not different. We conclude that, although the PRA and ANG II respond rapidly enough after hem to influence pituitary responses, the slightly greater responses of these factors to H2 are not responsible for greatly increased pituitary-adrenal responses to H2. On the other hand, the markedly potentiated vasopressin response to H2, which parallels that of ACTH, suggests that vasopressin may mediate the increased ACTH responses to H2.
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PMID:Potentiated cortisol response to paired hemorrhage: role of angiotensin and vasopressin. 254 52

Angiotensin II (ANG II) and vasopressin (AVP) are two powerful vasoconstrictors, and atrial natriuretic peptide (ANP) is a potent vasorelaxant. The changes in the density or affinity of binding sites for these agents that may alter target organ responsiveness in hypertension are reviewed. ANG II binding in mesenteric arteries was unaltered in one-kidney, one-clip (1-K, 1-C) and in 2-K, 1-C hypertensive rats, while in deoxycorticosterone acetate (DOCA)-salt hypertensive rats ANG II binding to blood vessels was significantly increased. A role of mineralocorticoids to increase the number of vascular ANG II sites in some hypertensive models is suggested. In spontaneously hypertensive rats (SHR) ANG II receptors were increased in young rats in the prehypertensive stage with respect to Wistar-Kyoto (WKY) control rats, but normal in older rats. AVP binding in the vasculature of hypertensive rats was uniformly decreased in inverse correlation to plasma AVP levels, but vascular responsiveness to AVP was exaggerated. Inositol trisphosphate production by blood vessels of SHR in response to AVP showed that increased AVP receptor-coupled phospholipase C activity may mediate in part the exaggerated pressor response in spite of reduced or normal density of receptors for vasoconstrictor peptides. Vascular ANP sites in 2-K, 1-C, 1-K,1-C, and DOCA-salt hypertensive rats varied inversely with plasma concentrations of ANP. Normal densities of ANP receptors in saralasin-sensitive 2-K, 1-C hypertensive rats correlated with ANP sensitivity, while saralasin-insensitive 2-K, 1-C hypertensive rats, which did not respond to ANP, had significantly decreased density of ANP vascular receptors.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Vascular receptors for angiotensin, vasopressin, and atrial natriuretic peptide in experimental hypertension. 255 50

The purpose of this study was to examine the influence of arterial baroreflexes on the pressor and regional hemodynamic responses to centrally administered angiotensin II (ANG II) in the conscious rat. Fourteen days after sinoaortic baroreceptor denervation (SAD) or the equivalent sham surgery, the pressor and hindquarters vascular resistance responses to intravenous administration of ANG II were augmented in the SAD group. The pressor and vasoconstrictor responses to intracerebroventricular ANG II were also augmented after SAD; however, the SAD animals were more than 1,000-fold more sensitive than the sham group to the pressor effects of intracerebroventricular ANG II. Further experiments demonstrated that 1) the enhanced pressor response to intracerebroventricular ANG II in the baroreceptor-denervated group was due to similar increases in sympathetic outflow and vasopressin mediated vasoconstriction, 2) the increased sensitivity to central ANG II occurs as soon as 1 h after SAD, and 3) the enhanced pressor effects to intracerebroventricular ANG II also occur with intracerebroventricular hypertonic saline. We conclude that arterial baroreflexes exert a potent central inhibitory effect on the central pressor actions of ANG II that are greater than can be accounted for by the peripheral reflex arc. Finally, because of the rapid onset of the increased responsiveness to central ANG II after SAD, we propose that baroreflex buffering of central pressor stimuli may be tonically involved in circulatory control.
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PMID:Baroreceptor denervation profoundly enhances cardiovascular responses to central angiotensin II. 256 57


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