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)

Experiments were carried out in conscious, unrestrained, male rats to evaluate possible interactions between brain prostanoids and the brain renin-angiotensin system in the control of vasopressin release and in cardiovascular regulation. The intracerebroventricular (icv) administration of prostaglandin D2 (PGD2) resulted in transient increases in the plasma vasopressin concentration (PAVP) and heart rate and a gradual increase in mean arterial blood pressure (MABP). Pretreatment icv with saralasin, an angiotensin II-receptor antagonist, moderately attenuated the vasopressin response to PGD2, but had no effect on the heart rate and blood pressure responses. Angiotensin II icv increased both PAVP and MABP. This vasopressin response was almost completely prevented by prior icv meclofenamate, a cyclooxygenase inhibitor, and the blood pressure response was attenuated. These observations, combined with previous studies of the role of central angiotensin II and central prostanoids in the physiological control of vasopressin release, suggest that there may be important interactions between brain prostanoids and the brain renin-angiotensin system in this control.
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PMID:Interactions between the brain renin-angiotensin system and brain prostanoids in the control of vasopressin secretion. 207 34

Physiological regulation of receptor-effector pathways is recognized as a significant factor determining target organ selectivity and sensitivity in several hormonal systems. Whether or not physiological regulation of the renal vasopressin (V2) receptor-effector pathway participates in the control of body fluid homeostasis is unknown. We evaluated four states likely to be associated with altered sensitivities of the renal V2 receptor-effector pathway as follows: dehydration (18-h hydropenia), volume expansion, exogenous arginine vasopressin (AVP) infusion (10 ng/kg + 0.25 ng.kg-1.h-1), and cyclooxygenase blockade (indomethacin, 2 mg/kg + 2 mg.kg-1.h-1) for effects on the antidiuretic efficacies and potencies of putative V2-receptor antagonists in conscious dogs. The antidiuretic efficacies of desGly9[Pmp1-D-Tyr(Et)2Val4]AVP [Smith Kline & French (SK&F) 101926; 0.01-1,000 micrograms/kg] ranged from that of a full agonist to that of an antagonist, depending on the physiological state studied. The vasopressin antagonist potency of SK&F 101926 was increased 150-fold in association with extracellular volume expansion and decreased by blockade of renal cyclooxygenase activity. This spectrum of activities is that anticipated for a partial agonist under conditions where receptor number and/or sensitivity of receptor-effector coupling is increased or decreased, respectively. Thus volume expansion and increased circulating vasopressin concentration are associated with effective decreases, whereas hydropenia and cyclooxygenase blockade are associated with effective increases in sensitivity of the renal V2 receptor-effector pathway in the dog kidney. We conclude that the V2 receptor-effector pathway is a site of integration of physiological mechanisms participating in the control of body fluid homeostasis in conscious dogs.
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PMID:Physiological regulation of the renal vasopressin receptor-effector pathway in dogs. 213 28

In vitro experiments on vascular smooth muscle often fail to reveal phenomena clearly demonstrable in vivo. Several recent observations in our laboratory have revealed the facility to uncover responses mediated by receptors whose functional expression had remained hidden with the standard experimental conditions first employed: conversely manipulation of conditions can selectively hide a particular receptor's response. Examples include the uncovering of responses to: 5HT1 receptors by raised O2 tension (via cyclooxygenase products) in human umbilical vessels; alpha 2-adrenoceptors in rabbit saphenous artery by angiotensin II and alpha 2-adrenoceptors in perfused rat tail by elevating tone with vasopressin. The powerful synergism of agonists which cannot on their own cause contraction, can lead to inaccurate interpretations of agonist-antagonist interactions. Finally, the influence of tissue metabolism on receptor expression clearly illustrates the complex processes which must be involved in vivo.
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PMID:Physiological modulation of alpha-adrenoceptor and 5HT receptor expression in blood vessels. 217 38

Vasoactive hormonal response to two levels of dietary protein intake was studied in seven healthy adult volunteers. The subjects were randomly placed on a 2-g.kg-1.day-1 (high) or 0.55-g.kg-1.day-1 (low) diet using a crossover design and were studied on the morning of the 5th day and again after 24 h of indomethacin treatment. Plasma renin activity (PRA), aldosterone, vasopressin, and urinary excretion of 6-ketoprostaglandin F1 alpha (PGF1 alpha) were significantly higher on the high-protein diet despite constancy of body weight, blood pressure, pulse, urinary sodium and potassium excretion, and plasma amino acid levels. After treatment with cyclooxygenase inhibitor indomethacin, 6-keto-PGF1 alpha excretion was equalized, but the elevated PRA and aldosterone levels persisted on the high-protein diet, suggesting that PRA and aldosterone elevations do not depend entirely on prostanoid release. We conclude that chronic augmentation of dietary protein intake is accompanied by alterations of vasoactive hormones, which persist for up to 10 h postprandially and are independent of elevated plasma amino acid levels. Such hormonal alterations may mediate some of the dietary protein-mediated changes in renal hemodynamics.
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PMID:Effects of dietary protein intake on vasoactive hormones. 218 41

Arachidonic acid (AA) is reported to be metabolized by three major pathways, i.e., cyclooxygenase (CO), lipoxygenase (LO), and NADPH-dependent cytochrome P450 monooxygenase (MO) pathways. Monooxygenase metabolites of AA have been proposed to play an important role in hormone action in various cells. Recently it was reported that the MO pathway may exist in rat liver. The present study was carried out to investigate the role of MO metabolites in vasopressin-induced glycogenolysis in isolated rat hepatocytes. The pretreatment of isolated rat hepatocytes with eicosatetraynoic acid (ETYA), an inhibitor of CO, LO, and MO pathways, and ketoconazole and SKF 525A, inhibitors of the MO pathway, dose-dependently reduced vasopressin-induced phosphorylase activation, while the pretreatment with indomethacin, an inhibitor of the CO pathway, had no effect. The increment of cytosolic calcium concentration in vasopressin-stimulated hepatocytes was also dose-dependently decreased by ETYA, ketoconazole, and SKF 525A. In vitro addition of epoxyeicosatrienoic acid (EET) dose-dependently increased both phosphorylase a activity and cytosolic calcium concentration. 14,15-EET was the most potent among four regioisomeric EETs. These results suggest that MO metabolites of AA, most likely EETs, may be involved in vasopressin-induced glycogenolysis probably via the activation of phosphorylase by increasing the cytosolic calcium concentration.
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PMID:Possible involvement of arachidonic acid metabolites of cytochrome P450 monooxygenase pathway in vasopressin-stimulated glycogenolysis in isolated rat hepatocytes. 236 26

Using rat renal papillary collecting tubule (RPCT) cells in culture, we examined the interactions of extracellular osmolality, vasopressin-stimulated cAMP, and prostaglandin E2 (PGE2) synthesis. Hypertonic solutions composed of equiosmolar amounts of urea and sodium chloride, 900-2,400 mosM, potentiated the increases of intracellular cAMP after vasopressin stimulation. Sodium chloride, rather than urea, was the important solute. The mechanism of this augmented cAMP response was complex, probably involving increased synthesis, decreased degradation, and reduced efflux of cAMP from the RPCT cells. The potentiating actions of hypertonic sodium chloride were specific for vasopressin-stimulated cAMP and were not observed for forskolin or PGE2-stimulated cAMP. Hypertonic solutions inhibited RPCT cell PGE2 production, and sodium chloride, rather than urea, was again the important solute. The enzymatic site of sodium chloride inhibition of PGE2 synthesis was apparently on the phospholipase enzymes, assessed by calcium ionophore and bradykinin stimulation, and not on cyclooxygenase, measured by arachidonic acid responsiveness. Reductions of osmolality, from 1,800 to 300 mosM, acutely increased PGE2 release, possibly through a calcium-dependent stimulation of phospholipase. We conclude that conditions that prevail in vivo during antidiuresis, namely hypertonicity of the papillary interstitium, may augment vasopressin responsiveness through increments of collecting tubule cAMP and reductions of PGE2 which could, in concert, maximize water reabsorption in the collecting tubule.
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PMID:Osmolality, vasopressin-stimulated cAMP, and PGE2 synthesis in rat collecting tubule cells. 242 57

Experiments were designed to determine the role of the endothelial cells and the metabolism of arachidonic acid in anoxic contractions of isolated canine basilar arteries. Rings, with and without endothelium, of these arteries were suspended for isometric tension recording; anoxia was induced by switching the mixture gassing the organ chamber from 95% O2-5% CO2 to 95% N2-5% CO2. In rings with endothelium, anoxia evoked increases in tension under basal conditions and during contractions to 5-hydroxytryptamine, uridine triphosphate, prostaglandin F2 alpha, and high K+. Under control conditions, these anoxic contractions were not prevented by alpha-adrenergic and serotonergic antagonists, by apyrase, or by inhibitors of cyclooxygenase. Anoxia prevented endothelium-dependent relaxations evoked by vasopressin and thrombin. In rings without endothelium, anoxia caused increases in tension during contractions evoked by various agonists, and in unstimulated preparations after inhibition of cyclooxygenase. Anoxic contractions were abolished by calcium entry blockers. These observations suggest that anoxic contractions of isolated canine basilar artery can be explained by the release of endothelium-derived contracting factor(s) and the accelerated entry of calcium in the smooth muscle cells, which possibly results from a diversion of arachidonic acid from the cyclooxygenase to the lipoxygenase pathway.
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PMID:Anoxic contractions in isolated canine cerebral arteries: contribution of endothelium-derived factors, metabolites of arachidonic acid, and calcium entry. 243 36

Pressor response to graded infusion of angiotensin II, noradrenaline, arginine-vasopressin, and serotonin and blood pressure change following indomethacin, an inhibitor of cyclooxygenase, were examined in conscious sheep, before and during the development of cyclosporin A-induced hypertension. Cyclosporin caused an increase in mean blood pressure from 68 +/- 2 to 82 +/- 3 mm Hg (p less than 0.001) and in heart rate from 67 +/- 4 to 91 +/- 4 beats/min (p less than 0.001). Pressor and heart rate responses to all substances tested were not changed by cyclosporin treatment suggesting that changes in pressor responsiveness are unlikely to be involved in the development of cyclosporin hypertension in sheep.
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PMID:Cyclosporin A and pressor responsiveness in sheep. 245 62

Cromakalim (BRL 34915), a K+ channel activator, and diltiazem relaxed isolated rat aortic rings contracted with a low KCl concentration (25 mM). Gilbenclamide (0.1-3 microM) did not modify base-line resting tension or responses to KCl but prevented the vasorelaxant effects of cromakalim without affecting those of diltiazem or nitrendipine. Cromakalim, in contrast to the latter compounds, did not relax aortic rings contracted with 55 mM KCl. In pentobarbital-anesthetized rats prepared for hemodynamic measurements with Doppler flow probes, a 20-min i.v. infusion of cromakalim (5.0 micrograms/kg/min) lowered mean carotid artery blood pressure. This effect reached maximum after administration and was accompanied by decreases in systemic (35%), hindquarter (45%), mesenteric (27%), and renal (19%) vascular resistances. The blood pressure effects of cromakalim were not modified by BW 755C (lipo and cyclooxygenase inhibitor), idazoxan, methylatropine, methysergide, promethazine, propranolol, SCH 23390 (DA-1 receptor antagonist), S-sulpiride, RP 59227 (antagonist of platelet activating factor receptors) or by bilateral vagotomy associated with ligation of carotid arteries. However, in rats pretreated with the hypoglycemic sulfonylureas glibenclamide or glipizide (20 mg/kg i.v.), cromakalim, in contrast to diltiazem or dihydralazine, failed to produce hypotension. In rats deprived of sympathetic drive by pithing, cromakalim produced only a minor fall in blood pressure; however, this effect became pronounced when the low base-line blood pressure of this preparation was elevated by an i.v. infusion of vasopressin and could be prevented by glibenclamide. In conclusion, cromakalim posseses a novel mechanism of vasorelaxation that is consistent with the activation of a cellular outward K+ current.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Vasorelaxant effects of cromakalim in rats are mediated by glibenclamide-sensitive potassium channels. 249 53

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)
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PMID:Prostaglandin I2 and the kidney. 251 64


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