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)

PGI2, or prostacyclin, and PGE2 are major derivatives of arachidonic acid. Arachidonic acid is converted by the cyclooxygenase enzyme to intermediate prostaglandin endoperoxides which are then enzymatically converted to PGI2 and PGE2 as well as to thromboxane A2 and PGF2 alpha. Aspirin and other nonsteroidal anti-inflammatory drugs inhibit the cyclooxygenase enzyme thereby reducing the amount of PGE2 and PGI2 produced. In the kidney, major stimuli of prostaglandin synthesis include vasoconstrictor hormones such as angiotensin II, vasopressin, endothelin and norepinephrine. Renal PGI2 and PGE2 synthesis is also increased after renal ischemia, immune injury to the kidney, and with renal parenchymal disease. Renal prostaglandin production also increases with severe arteriosclerotic cardiovascular disease, congestive heart failure, and severe hepatic disease. The increment of renal prostaglandin synthesis is important since PGI2 and PGE2 act as modulators of renal ischemia and vasoconstriction. The modulatory action leads to a negative feedback loop through which PGE2 and PGI2 and renal blood vessels in glomeruli reduce the vasoconstrictor action of the agonist, such as angiotensin II or norepinephrine. Nonsteroidal anti-inflammatory drugs can have nephrotoxic effects if they are used in clinical situations in which renal prostaglandin synthesis has increased compensatorily. In other words, the administration of indomethacin or other prostaglandin inhibitory drugs will reduce renal blood flow and glomerular filtration rate in patients with congestive heart failure, significant hepatic disease, or renal ischemia and vasoconstriction. PGI2 and PGE2 may have additional beneficial effects within the kidney in addition to being vasodilatory.(ABSTRACT TRUNCATED AT 250 WORDS)
Arch Mal Coeur Vaiss 1989 Nov
PMID:Prostaglandin I2 and the kidney. 251 64

Terlipressin (Glypressin) is a "pro-hormone"; after intravenous injection the glycyl radicals are slowly cleaved by enzymatic action, liberating vasopressin. We have assessed the efficacy of terlipressin in the treatment of severe hemoptysis. The study was performed on 20 patients: in 5 cases there was very copious hemoptysis and in 15 cases there was repeated hemoptysis of lesser volume. The cause was distributed as follows: 6 cases of neoplasms, 5 were sequelae of tuberculosis, bronchial dilatation 2 cases, pneumonia with abscess 2 cases, chronic airflow obstruction (COPD) 2 cases and 3 cases of silicosis. The treatment consisted of a slow intravenous injection of 2 mgm 4 times per day (9 patients), then in 11 patients an injection of 2 mgm at the time of acute episodes followed by 1 mgm every 6 hours. The patients received an average of between 15 and 20 mgm of the product for a treatment lasting over 5 days at the maximum. The results were as follows: total success 12 cases; partial success (a reduction to at least one-third of the initial hemoptysis): 5 cases; failure: 3 cases. The failures were linked in two cases to neoplastic disease and in one case there was an intolerance to the drug which did not allow the treatment to be pursued.(ABSTRACT TRUNCATED AT 250 WORDS)
Rev Mal Respir 1989
PMID:[Treatment of severe hemoptysis with terlipressin. Study of the efficacy and tolerance of this product]. 279 45

Using tritiated vasopressin, specific binding sites for vasopressin were identified on splenic membranes of Sprague-Dawley rats. One class of high affinity receptors was characterized with an equilibrium dissociation constant of 1.91 +/- 0.16 nM and a maximal binding capacity of 110 +/- 11 fmol/mg of protein. Several experimental evidences suggest that these receptors belong to the V1-vascular type: The affinity of 8 vasopressin agonists for the receptor is correlated to their vasopressor activity in vivo whereas no such relationship exists when their antidiuretic activity is considered. The affinity of 5 vasopressin antagonists for the receptor is correlated to their antivasopressor activity in vivo whereas no such relationship exists when their antidiuretic activity is considered. Vasopressin does not stimulate cyclic AMP production of splenic membranes. The regulation of these receptors was studied in sodium-sensitive (S) and sodium-resistant animals (R) of Dahl receiving a special diet (0.1 or 8% NaCl) for two weeks. In both strains of animals, the number of receptors is smaller in R animals than in S animals, whatever the diet ingested. Splenic membranes of rat bear easily accessible V1-vasopressinergic receptors. These receptors are modulated by sodium intake and the difference in receptor number between S and R rats could explain the increased vascular reactivity of S animals to vasopressin.
Arch Mal Coeur Vaiss 1986 Jun
PMID:[Regulation of V1-vasopressinergic receptors in the rat]. 302 72

We have previously shown that, injected s.c. to adrenalectomized Sprague-Dawley rats (SD.ADx), aldosterone has a mineralocorticoid specific effect on transmembrane movements of 22Na from arterial smooth muscle. These effects appear to be partly due to the action of an humoral factor. Indeed, in vitro, the late increase in passive 22Na efflux is not observed (Moura and Worcel, 1984). In rats perfused with a specific antagonists of the pressor effect of vasopressin (Vp), the in vivo administration of aldosterone induced a kinetic action similar to that observed after in vitro exposure to the mineralocorticoid. These results suggested that Vp may be the humoral factor (Moura, Angeli and Worcel, 1985). In adrenalectomized homozygous Brattleboro rats (DI.ADx), aldosterone (10(-8)M) increases ouabain independent 22Na efflux (DI.AX: 0.073 +/- 0.002 min-1(n = 15); DI.ADx + Aldo: 0.096 +/- 0.002 min-1(n = 12)p less than 0.01) and ouabain-dependent 22Na efflux (DI.ADx: 0.031 +/- 0.001 min-1; DI.ADx + Aldo: 0.037 +/- 0.002 min-1 p less than 0.01). Vp also increases ouabain sensitive and insensitive 22Na effluxes and potentiates the effects of aldosterone on passive Na+ transferts (DI.ADx + Aldo + Vp: 0.015 +/- 0.003 min-1 (n = 16) p less than 0.01). In conclusion, these results suggest that Vp may be involved in the effects of aldosterone on 22Na effluxes. Furthermore Vp potentiates the effects of aldosterone on passive 22Na effluxes. But it is not yet possible to ascertain if Vp action is additive or permissive.
Arch Mal Coeur Vaiss 1986 Jun
PMID:[Effects of aldosterone and vasopressin on transmembrane efflux of sodium from the arterial wall]. 309 13

We have previously shown that an humoral factor is involved in the delayed effect of aldosterone on the passive transmembrane movements of Na+ from arterial smooth muscle (Moura and Worcel, 1984). In absence of vasopressin, the effects of aldosterone on the same Na transports suggest that vasopressin may be this humoral factor (Moura, Angeli and Worcel, 1986) (Angeli, Moura and Worcel, 1986). We show here that the s.c. injection of aldosterone (10 micrograms/kg) to adrenalectomized Sprague Dawley rats induces a release of vasopressin. This peptide exerts a direct action on ouabain-sensitive and insensitive components of 22Na efflux from the rat tail artery, and potentiates the late effect of aldosterone on passive Na+ efflux. There is no additive effect of the two hormones on Na+ pump activity. In conclusion vasopressin is the humoral factor involved in the late effect of aldosterone on passive transmembrane movement of Na from vascular smooth muscle.
Arch Mal Coeur Vaiss 1987 Jun
PMID:[Involvement of vasopressin in the effects of aldosterone on the arterial wall]. 311 78

The role of circulating bradykinin in the regulation of cardiovascular homeostasis was studied in the normotensive conscious rat using a competitive antagonist of bradykinin at the receptor level. This antagonist (B4162) was administered intravenously as a bolus dose of 400 micrograms. This dose was shown to effectively block the hypotensive effect of exogenous bradykinin (2.5 micrograms) for at least 5 min. The bradykinin antagonist was administered at the end of an infusion of angiotensin II (1 ng/min, n = 5, or 12.5 ng/min, n = 6), of methoxamine (0.5 micrograms/min, n = 5, or 4 micrograms/min, n = 6), of lysine vasopressin (0.25 mUI/min, n = 11) or of saline (10 microliter/min, n = 7). The bradykinin antagonist did not change the mean arterial pressure of the control rats. The low doses of angiotensin II and of methoxamine did not have an effect on mean blood pressure. The bradykinin antagonist however increased mean blood pressure of these rats within 1 min by 10 +/- 2 (p less than 0.01, mean +/- SEM) and by 12 +/- 3 (p less than 0.01) mmHg, respectively. The large dose of angiotensin II raised mean blood pressure from 127 +/- 3.6 to 142 +/- 4.9 mmHg and that of methoxamine from 130 +/- 2 to 146 +/- 5 mmHg.(ABSTRACT TRUNCATED AT 250 WORDS)
Arch Mal Coeur Vaiss 1987 Jun
PMID:[Attenuation of the vasopressor effect of angiotensin II, vasopressin and alpha 1-adrenergic stimulation by bradykinin]. 311 81

Endothelial cells of the arterial wall can generate vasodilator and vasoconstrictor substances. The prototype of a vasodilator substance formed primarily in the endothelium is prostacyclin, although its main target under physiological conditions are the platelets. In addition, the endothelial cells respond to a variety of neurohumoral mediators by the liberation of an unidentified substance(s) (endothelium-derived relaxing factor) with a potent inhibitory effect on vascular smooth muscle, presumably because it accelerates the production of cyclic GMP in the latter. Endothelium-derived relaxing factor is very unstable, and has an extremely short half-life. It is inactivated by plasma proteins and thus does not fulfill a hormonal role. A metabolite of arachidonic acid may be involved in the production of endothelium-derived relaxing factor. Among the neurohumoral mediators which release it are: acetylcholine (through activation of muscarinic receptors), adenosine di- and triphosphate (P2-purinergic receptors), bradykinin, histamine (H1- or H2-histaminergic receptors, depending on the species), serotonin (S1-serotonergic receptors), substance P, oxytocin, thrombin and vasopressin (V1-vasopressinergic receptors). The release of the factor can also be triggered by aggregating platelets (because they release adenine nucleotides and serotonin) and by increases in shear stress. It is likely that endothelium-dependent dilatation helps to prevent intraluminal coagulation in arteries with a normal intima. Absence, or dysfunction of the endothelium may favor the occurrence of vasospasm. Endothelium-dependent relaxations are reduced in atherosclerotic blood vessels.(ABSTRACT TRUNCATED AT 250 WORDS)
J Mal Vasc 1986
PMID:[The endothelium and arterial reactivity]. 349 May 30

Tobacco smoking increases the risk of myocardial infarction and sudden death. When used for diagnostic and therapeutic ends, vasopressin, at low doses, may induce acute ischaemic complications in patients with coronary artery disease. This study showed that in some patients the inhalation of tobacco smoke caused a rise in plasma vasopressin and nicotine-stimulated-neurophysin, a substance easily measured and used as a marker of vasopressin secretion because of the close relationship of the two substances. Twelve out of twenty five subjects presented higher levels of nicotine-stimulated-neurophysin than the normal for the same group before smoking (p less than 0,005): 280 +/- 54 compared to 714 +/- 459 pg/ml. Simultaneous measurement of vasopressin and nicotine-stimulated-neurophysin every 5 minutes in 4 subjects confirmed the parallel changes of these substances during smoking. These results suggest that vasopressin may play a primary role in the acute ischaemic complications of tobacco smoking. The concept of the "vasopressin response" could be used as a biological parameter to identify subjects at "high cardiovascular risk" under the effects of tobacco and so lead to a prophylactic strategy aimed more specifically at these patients.
Arch Mal Coeur Vaiss 1984 Jan
PMID:[Possible role of vasopressin in ischemic accidents related to tobacco consumption]. 642 96

Previously we reported that AVP is a potent vasoconstrictor in the TYRODE's perfused rat kidney. In vivo however AVP elicited only minor effects on renal blood flow. We hypothetized that differences in shear stress, particularly related to differences in viscosity could be involved. In this study, we investigate the role of perfusate viscosity in the modulation of AVP-induced renal vasoconstriction by NO. Experiments were performed in kidneys isolated from male Sprague-Dawley rats (220 g). Kidneys were perfused at a constant flow of 8 mL/min, in a recirculating system, with TYRODE's solutions supplemented with 6% bovin serum albumin (BSA) or 4.7% Ficoll 400 (Ficoll). The viscosities relative to water were respectively of 1.33 (BSA), 2.32 (Ficoll) and 1.03 (TYRODE). Concentration-response curves to AVP were constructed in the absence or presence of 100 microM N omega-nitro-L-arginine (L-NA), an inhibitor of NO synthase, and compared to those obtained in kidneys perfused with TYRODE's solution. AVP elicited a concentration-dependent renal vasoconstriction, with a progressive shift of the curves to the right and a small decrease in the maximum response when the kidneys were perfused with perfusates of increasing viscosities: logEC50 = -9.9 +/- 0.1 (TYRODE, n = 14), -9.7 +/- 0.1 (BSA, n = 5), -9.0 +/- 0.1 (Ficoll, n = 5) (m +/- e.s.m. Anova, p < 0.001); Emax = 34 +/- 1, 31 +/- 2 and 26 +/- 3 mmHg/mL/min (Anova, p < 0.001). L-NA abolished the differences between kidneys perfused with solutions of different viscosities in logEC50 for vasopressin (10.3 +/- 0.1, 10.4 +/- 0.1 and 10.5 +/- 0.1, n = 5-11, Anova, NS) but did not affect Emax values. In conclusion, present results show that 1) AVP-induced renal vasoconstriction is modulated according to the viscosity of perfusate and 2) NO is involved in this effect. Viscosity, a major determinant of shear stress, should be considered in hemodynamic studies performed on isolated kidneys.
Arch Mal Coeur Vaiss 1998 Aug
PMID:[Modulation by nitric oxide of vasopressin induced renal vasoconstriction varies with perfusate viscosity in the isolated rat kidney]. 974 70

Pharmacovigilance data have reported some cases of arterial hypertension in patients treated with serotonin reuptake inhibitors. This side effect is now called serotonin syndrome. Moreover, some authors have shown that these drugs could reduce, at least in part, the fall in blood pressure (BP) observed in experimental models or in human forms of orthostatic hypotension, suggesting a modulation of the autonomic nervous system by these drugs. These data led us to study in freely moving Wistar rats the mechanisms involved and the putative involvement of autonomic nervous system. Intracerebroventricular (i.c.v.) administration of fluoxetine (5-50 micrograms) induced an increase in BP similar to which was obtained following central administration of serotonin (5-HT) (0.5-5 micrograms). After 5-HT, the pressor effect was immediate (1 min following injection) and involved the baroreflex pathway (bradycardia). The fluoxetine-induced pressor response reached its maximal 1 hour after injection without any significant change in heart rate (HR). At the dose of 10 micrograms i.c.v., fluoxetine significantly increased mean BP by 16 +/- 4 mmHg. This pressor response was partially but significantly reduced by a pretreatment by the alpha 1-adrenoreceptor antagonist, prazosin (500 micrograms.kg-1 i.v.) (+7 +/- 4 mmHg, p < 0.05) or by a V1A-vasopressin receptor antagonist (20 micrograms.kg-1 i.v.) (+5 +/- 3 mmHg, p < 0.05). However, pretreatment by the beta-adrenoreceptor antagonist, propranolol (1 mg.kg-1 i.v.) and the antagonist 5-HT2, ketanserine (5 mg.kg-1 i.v.) did not modify the fluoxetine-induced pressor response. In freely moving rats receiving fluoxetine (10 micrograms i.c.v.), vasopressin plasma levels were significantly higher (+39 +/- 5 pg.mL-1) than in rats receiving saline (100 microL i.c.v.) (+14 +/- 4 pg.mL-1), thus confirming the involvement of vasopressinergic mechanisms in the fluoxetine-induced pressor response. These data suggest that in freely moving Wistar rats, central acute administration of fluoxetine induces a pressor response mediated by both an increase in sympathetic tone and a vasopressin release. This observation could suggest the putative use of alpha 1-adrenoreceptors antagonists and/or V1A-vasopressin receptor antagonists in the treatment of the serotonin syndrome.
Arch Mal Coeur Vaiss 1999 Aug
PMID:[Reduction of the pressor effect of fluoxetine after V1A-vasopressin receptor blockade in the conscious rats]. 1048 51


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