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)

In hypoosmolar hyponatremia, vasopressin is commonly observed to be less than maximally suppressed. This is attributed to the presence of nonosmolar vasopressin stimuli. However, the exact relationship of nonsuppressed antidiuretic hormone to specific circulatory parameters is controversial. Therefore, in the present study, we examined this question in 100 hypoosmolar hyponatremic patients in the Department of Medicine. Despite plasma hypoosmolality, vasopressin was found to be measurable in 92% of patients. Seventy patients suffered from edematous disorders (congestive heart failure, cirrhosis) or volume contraction per se; in these patients we observed unequivocal, though indirect, evidence of advanced circulatory alterations. These were associated with hyponatremia and nonsuppressed vasopressin. However, the latter could not be related directly to a specific circulatory parameter such as mean arterial blood pressure, creatinine clearance, plasma renin activity (PRA), norepinephrine, or aldosterone. However, patients with nondetectable vasopressin (n = 8) differed significantly from those with high vasopressin concentrations (n = 8: PADH greater than 9 pg/ml); in the latter, pulse rate (104 +/- 3 vs. 82 +/- 5 beats/min), plasma urea concentration (90 +/- 5 vs. 32 +/- 5 mg/dl), plasma urate concentration (7.2 +/- 0.8 vs. 3.6 +/- 0.8 mg/dl), and PRA (36 +/- 7 vs. 9.5 +/- 4.6 ng AI/ml/h) were all significantly higher than in the former. It is concluded that, in hyponatremia, the relationship between circulatory impairment and vasopressin is complex.
J Cardiovasc Pharmacol 1986
PMID:Vasopressin in hyponatremia: what stimuli? 243 81

The hemodynamic and hormonal changes produced by adriamycin-induced cardiomyopathic congestive heart failure in rabbits were studied. Adriamycin cardiomyopathy in rabbits led to ventricular dilatation, pleural and pericardial effusions, hepatic congestion, and ascites. These pathological changes were associated with the maintenance of a normal blood pressure but a lowered cardiac output and increased total peripheral resistance. Plasma renin activity and plasma norepinephrine were increased twofold in rabbits with congestive cardiac failure. However, plasma vasopressin and osmolality were normal, whereas an increased vascular sensitivity to the infusion of exogenous vasopressin was demonstrated. Despite the normal levels of plasma vasopressin, administration of a specific vascular vasopressin antagonist led to a fall in blood pressure, a significant increase in cardiac output, and a decrease in total peripheral resistance. No such hemodynamic changes occurred on infusing normal rabbits with the vascular vasopressin antagonist, nor did any significant hemodynamic changes occur on injecting vehicle in rabbits with heart failure. These results suggest that in adriamycin-induced cardiomyopathic heart failure in rabbits, there is activation of the renin-angiotensin system and the sympathetic nervous system together with an increased sensitivity to vasopressin. These three hormonal systems help to maintain blood pressure by increasing total peripheral resistance in this experimental model of heart failure.
J Cardiovasc Pharmacol 1986
PMID:Role of vasopressin in experimental congestive cardiac failure. 243 82

Superior mesenteric arterial flow, arterial pressure, and heart rate were recorded, and plasma arginine-vasopressin (AVP) concentration was measured, during intravenous infusions of AVP (0.1-8.1 mU X kg-1 X min-1) in conscious unrestrained cats under two experimental situations--when autonomic function remained intact and, on other days, when it had been impaired by pretreatment of the animals with the ganglionic blocking agent pentolinium tartrate (2.5 mg X kg-1 and 0.125 mg X kg-1 X min-1). The dose-related increases in the plasma concentrations of AVP attained during the infusions of the peptide were similar under the two experimental situations. The curve expressing the relationship between the dose of AVP and the decrease in superior mesenteric arterial conductance (ml X min-1 X kg-1 X mm Hg-1) for when ganglia were blocked was similar to the curve for when autonomic function remained intact. Elevations in the circulating levels of the peptide within the physiological range (less than 30 fmol X ml-1) were associated with significant decreases in conductance, both when ganglia were blocked and when they were intact. In contrast to conductance, the curve expressing the relationship between the dose of AVP and the increase in arterial pressure for when ganglia were blocked was displaced markedly to the left when compared with the curve for when reflexes remained intact, even though the effect of ganglion blockade on pressor responses did not reach statistical significance with the two lowest doses of AVP.(ABSTRACT TRUNCATED AT 250 WORDS)
J Cardiovasc Pharmacol 1987 Mar
PMID:Sensitivity of intestinal resistance vessels to vasopressin after ganglionic blockade in the conscious cat. 243 4

The effects of divalent cations on human platelet vasopressin receptor binding characteristics and effects of receptor occupancy on endogenous protein phosphorylation were investigated. Binding of vasopressin to its receptor is modulated by both the nature and the concentration of ions. Whatever the cation present, guanosine 5'-triphosphate or 5' guanylylimidodiphosphate do not alter the receptor binding characteristics. In the presence of extracellular calcium, vasopressin stimulates the phosphorylation of a 45,000-dalton protein and to a lesser degree of a 20,000-dalton protein following a pattern observed with thrombin and 12-O-tetradecanoylphorbol-13-acetate, a phorbol ester. Phosphorylation is also stimulated by a V1 vascular agonist, but not V2 renal agonists, and is more potently blocked by a V1 vascular antagonist than by a V2 renal antagonist. These results suggest that human platelets bear typical V1 vascular vasopressin receptors which stimulate the phosphorylation of specific substrates of protein kinase C and myosin light-chain kinase.
J Cardiovasc Pharmacol 1987 Jul
PMID:The human platelet vasopressin receptor and its intracellular messengers: key role of divalent cations. 244 Nov 50

Atrial natriuretic peptides (ANPs) have been implicated in volume homeostasis and blood pressure regulation; however, little is known about factors regulating the release of ANPs. We therefore examined the roles of the sympathetic and parasympathetic nervous systems, the renin-angiotensin system, and vasopressin in the release of ANPs, under basal conditions and after acute blood volume expansion or acute salt loading in conscious rats. Plasma concentrations of immunoreactive ANPs (ir-ANPs) were measured by specific radioimmunoassay. Both acute blood volume expansion and acute salt loading increased basal plasma levels of ir-ANPs (90.4 +/- 5.2 pg/ml) four- to fivefold within 2 min. Basal and stimulated plasma levels of ir-ANPs were unaltered by pretreatment with methylatropine or with propranolol or by ganglionic blockade with hexamethonium. Total adrenergic blockade (combined treatment with yohimbine, prazosin, and propranolol) had no effect on basal or salt loading-stimulated plasma levels of ir-ANPs and slightly attenuated blood volume expansion-induced release of ANPs. Ganglionic blockade with chlorisondamine tripled basal plasma concentrations of ir-ANPs but had no effect on stimulation-induced release of ANPs. Acute blockade of the renin-angiotensin system with captopril or infusion of saralasin or pretreatment with a vasopressin pressor antagonist had no effect on basal or stimulated release of ANPs. Following intravenous bolus injections of graded doses of l-norepinephrine, angiotensin II, and vasopressin, mean arterial pressure and plasma levels of ir-ANPs increased in a dose-dependent manner. In conclusion, plasma concentrations of ir-ANPs can be acutely elevated by several physiological stimuli: volume expansion; salt loading; and pressor hormones.(ABSTRACT TRUNCATED AT 250 WORDS)
J Cardiovasc Pharmacol 1987 Oct
PMID:Role of autonomic nervous system and vasoactive hormones in the release of atrial natriuretic peptides in conscious rats. 244 95

The present study was designed to assess in conscious normotensive rats the influence of various pressor agents on the acute blood pressure response to a bradykinin antagonist (B4162). This antagonist was used at a dose (400 micrograms i.v.) which had been previously shown to block the blood pressure lowering effect of exogenous bradykinin for several minutes. In control rats, the bradykinin antagonist had no effect on blood pressure. However, in rats pretreated with nonpressor doses of angiotensin II or methoxamine or with pressor doses of vasopressin or methoxamine, the same antagonist significantly increased blood pressure by 10 +/- 2.2, 12 +/- 2.7, 9 +/- 1.7, and 16 +/- 3.4 mm Hg, respectively. It therefore appears that circulating bradykinin is not directly involved in blood pressure regulation of conscious normotensive rats. Endogenous bradykinin may however play an important role in blood pressure control by attenuating the pressor effect of angiotensin II, vasopressin, and alpha-adrenoceptor stimulation.
J Cardiovasc Pharmacol 1988 Jan
PMID:Influence of endogenous bradykinin on acute blood pressure response to vasopressors in normotensive rats assessed with a bradykinin antagonist. 245 Feb 56

Conscious dogs instrumented for the measurement of arterial pressure and cardiac output (electromagnetic flowmeter) received intravenous injections of 4-valine-8-D-arginine vasopressin (VDAVP) and 1-deamino-8-D-arginine vasopressin (dDAVP), two specific antidiuretic agonists. Both agents led within minutes to dose-dependent increases in cardiac output and heart rate, as well as to decreases of total peripheral resistance and mean arterial pressure. Indomethacin did not affect the hemodynamic responses to VDAVP administration. The analog 8-arginine-9-desglycinamide vasopressin, which retains behavioral effects of vasopressin but is a weak antidiuretic agonist, showed only weak hemodynamic effects that were similar in nature to those of VDAVP and dDAVP. Thus, the capability to increase cardiac output and decrease peripheral resistance appeared to correlate best with the antidiuretic activity of the three vasopressin analogs tested. We also observed that pretreatment of dogs with a combined vasopressor (V1) and antidiuretic (V2) vasopressin antagonist completely prevented the increase in cardiac output that is normally associated with the infusion of arginine-vasopressin, 10 ng kg-1 min-1, after V1 blockade. Our results confirm the existence of powerful, dose-related hemodynamic effects of various antidiuretic agonists in conscious dogs; these effects being opposite to those normally elicited by arginine-vasopressin.
J Cardiovasc Pharmacol 1988 Feb
PMID:Characterization of acute hemodynamic effects of antidiuretic agonists in conscious dogs. 245 11

In pentobarbital-anesthetized rats prepared for hemodynamic measurements with Doppler flow probes, intravenous (i.v.) infusions of fenoldopam (2.5 - 160.0 micrograms/kg/min during 15 min) decreased mean carotid artery blood pressure, total peripheral, hindquarter, renal, and mesenteric vascular resistances and increased renal blood flow strongly. The hypotensive effects attained a maximum within the first 3 min of infusion but waned by greater than 30% at the end of fenoldopam administration. This tolerance was observed for calculated total peripheral and hindquarter vascular resistances and to a lesser extent for mesenteric resistance. However, it was absent on the renal vascular bed. Pretreatment with either enalapril, pepstatine, or bilateral nephrectomy significantly increased the hypotensive response to fenoldopam and attenuated the development of tolerance. In conscious spontaneously hypertensive rats (SHR), enalapril potentiated strongly the small blood pressure-lowering activity of fenoldopam. The fall in blood pressure produced by fenoldopam was specifically blocked by SCH 23390, an antagonist of DA-1 dopamine receptors. In normotensive vasopressin-supported pithed rats given phenoxybenzamine plus propranolol, fenoldopam, like SCH 23390, blocked the vasodepressor effects of i.v. bolus injection of dopamine and fenoldopam. In pithed rats, fenoldopam evoked a pressor response that was significantly reduced by enalapril, SCH 23390, or bilateral nephrectomy. In conclusion, fenoldopam exerts DA-1 agonist and antagonist effects. The latter property, together with the activation of the renin-angiotensin system, appears to be responsible for the development of tolerance to the fenoldopam evoked-hypotension. The lack of a tolerance at the level of the renal vascular bed is possibly due to the existence of a large population of DA-1 receptors in this region.
J Cardiovasc Pharmacol 1988 Apr
PMID:Studies on the mechanisms of the development of tolerance to the hypotensive effects of fenoldopam in rats. 245 48

Whether or not the central nervous system is involved in the genesis of hypertension in an individual patient, it becomes a major determinant of the responses to antihypertensive therapy once a treatment strategy is adopted. The major mechanisms through which the central nervous system influences blood pressure are sympathetic and parasympathetic nervous system activity and vasopressin release, either together or separately, but additional mechanisms may also contribute. When vasodilators are used, for example, the reactive increase in plasma catecholamines makes a substantial contribution to limiting the blood pressure fall. The sympathetic activation may lead to the reactive increase in plasma renin activity and sodium retention, which also plays an important role in limiting the antihypertensive action. Among newer agents, the effectiveness of calcium channel blockers could reflect a special action on the central nervous system that may contribute to reducing the reactive vasopressor responses. Treatment strategies that address the problem of the central nervous responses are more likely to be effective than approaches that avoid or ignore it.
J Cardiovasc Pharmacol 1987
PMID:The central nervous system and effective antihypertensive effects of a calcium channel blocker. 245 13

The roles of vasopressin and angiotensin II in the regulation of peripheral vascular tone were investigated in control rats and in rats with chronic (15 weeks) aortic stenosis, by intravenous application of a specific antagonist to the vascular receptors of vasopressin and the angiotensin-converting enzyme inhibitor teprotide. The application of a Silver clip (0.6 mm) on the aorta ascendens produced a hemodynamically effective aortic stenosis with an increase in left ventricular weight (38%), a reduction in mean arterial pressure, cardiac index, and stroke volume index, and an increase in peripheral vascular resistance. In both groups of rats, a bolus injection of 30 micrograms of the vasopressin inhibitor d (CH2) 5 Tyr (Me) arginine vasopressin (AVP) showed an agonistic effect by increasing arterial pressure by 11 and 15 mm Hg, respectively, and no antagonistic effect in the control animals. In the rats with chronic aortic stenosis we observed a significant fall in blood pressure (4.1 +/- 5.5 mm Hg; p less than 0.05) and a reduction in peripheral vascular resistance of 6.3% (p less than 0.02). Stroke volume index and heart rate did not change. Most of the animals with aortic stenosis had inappropriately elevated plasma levels of vasopressin and increased levels of plasma renin concentration. The rats with aortic stenosis and inappropriately increased values of vasopressin showed significantly lower plasma osmolality, cardiac index, and stroke volume index and increased peripheral vascular resistance compared with the stenosed rats with a normal osmoregulation of vasopressin.(ABSTRACT TRUNCATED AT 250 WORDS)
J Cardiovasc Pharmacol 1988 May
PMID:Vasoconstrictor role of vasopressin and angiotensin in experimental aortic stenosis in the rat. 245 39


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