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)

We compared the effects of three vasoactive peptides (angiotensin II, vasopressin, and bradykinin) and norepinephrine on the production of prostaglandin I2 [prostacyclin (PGI2)] and PGE2 by isolated rat adipocytes. Angiotensin II, vasopressin, and bradykinin stimulated PGI2 production but had minimal or no effect on PGE2 production or triglyceride lipolysis in isolated rat adipocytes, while norepinephrine stimulated PGI2 production, PGE2 production, and triglyceride lipolysis. The arachidonic acid that serves as substrate for PGI2 production in adipocytes in response to the vasoactive peptides appears to be derived from the cellular phospholipids rather than the triglycerides in these triglyceride-laden cells. The adipocyte contains two separate mechanisms for PG production: 1) a catecholamine-stimulated mechanism for the production of PGI2 and PGE2 that is activated concomitantly with triglyceride lipolysis, and 2) a mechanism activated by vasoactive peptides for the stimulation of PGI2 production independent of triglyceride lipolysis and PGE2 production. These mechanisms may have distinct functions.
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PMID:Stimulation of prostacyclin production in isolated rat adipocytes by angiotensin II, vasopressin, and bradykinin: evidence for two separate mechanisms of prostaglandin synthesis. 388 13

Sympathetic neurotransmission can be modulated by prostaglandins in a number of tissues, but it is not known whether thromboxane A2 also influences neurotransmission. In this study, vasoconstrictor responses to electrical stimulation of the sympathetic nerves and to injection of noradrenaline were examined in the blood perfused mesentery of the rat in situ. The thromboxane synthetase inhibitor dazoxiben, infused into the perfusion circuit at 10-100 mumol/l, significantly inhibited constrictor responses to nerve stimulation and to injected noradrenaline and vasopressin. The cyclo-oxygenase inhibitor indomethacin (28 mumol/kg intravenously) had no effect on responses to nerve stimulation or noradrenaline, but pretreatment with indomethacin abolished the inhibitory effect of dazoxiben on vasoconstrictor responses. The thromboxane-mimetic (U46619, 10 nmol/l) slightly reduced responses to nerve stimulation (but not to noradrenaline), whereas prostacyclin (3-10 nmol/l) and PGE2 (3 nmol/l) markedly reduced responses both to nerve stimulation and to injections of noradrenaline. These prostanoids did not alter perfusion pressure at these concentrations. The data suggest that the inhibitory effect of dazoxiben on sympathetic neurotransmission is unlikely to be due directly to inhibition of thromboxane synthesis. Inhibition might result from diversion of endoperoxide metabolism to endogenous prostanoids that, in turn, inhibit activation of vasoconstrictor mechanisms.
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PMID:Inhibition of vasoconstrictor mechanisms by dazoxiben in the rat mesenteric vasculature. 392 37

The cardiorespiratory, sympathetic and biochemical effects of T-2 toxin were examined in conscious rats and guinea pigs. The pithed rat preparation was also used to evaluate possible direct effects of T-2 on the heart and vasculature. Injection of T-2 (0.5-2.0 mg/kg i.v.) into conscious rats produced prolonged (6-8 hr) hypertension and tachycardia, followed by hypotension. Total peripheral resistance was increased and cardiac output decreased. In guinea pigs, a steady decrease in pressure and rate occurred. Intravenous administration of T-2 to pithed rats did not alter blood pressure or heart rate at a time when, in conscious rats, both blood pressure and heart rate were increased. Significant elevations of arterial plasma norepinephrine, epinephrine and dopamine occurred after T-2, with metabolic acidosis, hypocarbia and hyperoxemia in both conscious rats and guinea pigs. In the rat, increase in plasma vasopressin and prostacyclin were elevated, but thromboxane and leukotriene C4-immunoreactivity were not changed. In pithed rats, T-2 did not increase basal or stimulated plasma catecholamines but produced the same changes in blood gases, pH and lactate. The LD50 values for i.v. T-2 in the rat and guinea pig were 0.74 and 1.30 mg/kg, respectively. The data are consistent with the hypothesis that T-2 toxin disrupts cellular aerobic metabolism, resulting in lactic acidosis, sympathoadrenomedullary activation, variable initial circulatory responses and eventual cardiovascular collapse.
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PMID:Cardiorespiratory, sympathetic and biochemical responses to T-2 toxin in the guinea pig and rat. 397 27

Prostacyclin (PGI2) and prostaglandin E2 (PGE2) production by rat glomerular epithelial cells in culture were stimulated by arginine vasopressin (AVP) over a dose range of 10(-9) to 10(-6) M, but only if the cells were allowed to recover from trypsin treatment. The effect of AVP was related to its pressor activity since the antidiuretic analogue of AVP, 1-deamino-8-D-Arg-vasopressin (dDAVP) had no effect. Angiotensin II and kallidin (lysyl-bradykinin) did not affect prostaglandin production by these cells. The stimulatory effect of AVP on arachidonate metabolism was inhibited by the calcium channel antagonist, nifedipine, in a dose-dependent fashion suggesting that cellular uptake of calcium was required.
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PMID:Stimulation of prostaglandin production in rat glomerular epithelial cells by antidiuretic hormone. 608 84

Acute hypovolemia induced by bleeding (5 ml/300 g body weight) halothane-anesthetized (0.8% in oxygen) rats is attended by hypotension, bradycardia, and increases in plasma renin, vasopressin, and catecholamine levels. Infusion of prostacyclin (PGI2, O.03 microgram/kg.min) to acutely hemorrhaged rats enhanced recuperation of heart rate, and potentiated the sympathetic response and vasopressin release without altering blood pressure of plasma renin concentration (PRC). Bleeding of bilaterally adrenal demedullated, splanchnicectomized rats resulted in prolonged hypotension and increased plasma levels of vasopressin and renin; epinephrine in the plasma was not detectable, and plasma norepinephrine concentration was not increased after hemorrhage. Prostacyclin infusion to the demedullated, splanchnicectomized rats had no effect on heart rate but enhanced blood pressure recovery after hemorrhage; in this experimental group, PRC was markedly elevated but prostacyclin had no effect on plasma vasopressin or catecholamine concentrations. In rats exposed to severe bleeding, resulting in a nonreversible shock and high mortality, PGI2 infusion after the bleeding increased the survival rate without effect on blood pressure, heart rate, or circulating levels of vasopressin and catecholamines. This study suggests that prostacyclin, through stimulation of the sympathoadrenal axis, enhances heart rate recuperation and vasopressin release in response to acute hemorrhagic shock. Furthermore, prostacyclin may stimulate renin secretion in sufficient amount to compensate for the inadequate sympathetic response during hemorrhagic shock. It is also shown that prostacyclin improves the survival rate to severe hemorrhage without overt hemodynamic or sympathetic effects.
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PMID:Alteration of cardiovascular, neurogenic, and humoral responses to acute hypovolemic hypotension by administered prostacyclin. 617 8

The effects of prostaglandins of the E series on sodium and water transport have been studied extensively. PGE2 has been shown to inhibit the increase in osmotic water flow produced by vasopressin and to stimulate short-circuit current (SCC) in the toad bladder. On the other hand, the effects of prostacyclin (PGI2), an arachidonic acid product, on sodium and water transport have not been extensively evaluated. The present studies describe the effects of PGI2 on basal and vasopressin-stimulated osmotic water flow and on SCC in the urinary bladder of the toad. Studies were performed in the absence or presence of indomethacin. PGI2 in the absence of indomethacin had no effect on basal or vasopressin-stimulated osmotic water flow. When indomethacin was present, thereby eliminating intrinsic prostaglandin biosynthesis, PGI2 inhibited basal but not vasopressin-stimulated osmotic water flow. PGI2 increased SCC in the presence or absence of indomethacin. 6-keto PGF1 alpha, the stable metabolite of PGI2, had no effect on SCC. PGI2 stimulated cAMP production in isolated toad bladder epithelial cells. 2',5'-Dideoxyadenosine, an inhibitor of cAMP production, blocked the increase in SCC produced by PGI2, suggesting that the effects of this compound on SCC are mediated via cAMP.
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PMID:Effects of prostacyclin on short-circuit current and water flow in the toad urinary bladder. 618 21

A chemically stable carboprostacyclin analogue, ZK 36374 has been compared with two other prostacyclin derivatives with respect to ADP-induced in vitro aggregation of baboon and human platelets and ex vivo platelet aggregation in the baboon. ZK 36374 was also tested on the systemic arterial blood pressure of the baboon and against vasopressin-induced ECG changes in primates. Compared to the other two compounds, ZK 36374 displayed enhanced anti-platelet aggregating activity; there was dissociation between this property and its hypotensive potency. ZK 36374 antagonized the vasopressin-induced ECG changes. These results indicate that ZK 36374 possesses therapeutic potential in vascular disease including that affecting the coronary vessels.
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PMID:Inhibition of platelet aggregation and antagonism of vasopressin-induced ECG changes in primates by a carboprostacyclin analogue, ZK 36374. 620 Sep 48

The present study examined the involvement of prostaglandins (PGs) in the mechanisms of ACTH and beta-endorphin release from rat anterior pituitary quarters incubated in vitro. Various cyclooxygenase inhibitors (indomethacin, diclofenac, flurbiprofen) had no effect on basal release of ACTH-like or beta-endorphin-like immunoreactivity (beta-EI), but enhanced ACTH-immunoreactivity/beta-EI release upon stimulation by arginine-vasopressin (AVP) or synthetic ovine corticotropin-releasing factor [CRF-(1-41)]. The lowest effective concentration of indomethacin was just sufficient to prevent PG synthesis. Indomethacin was similarly active after blockade of the phosphodiesterase by 3-isobutyl-1-methylxanthine. When added to the incubation media in concentrations up to 1 microM, PGE2, D2, F2 alpha, or prostacyclin (PGI2) did not alter basal beta-EI release; however, with stimulation by AVP or CRF-(1-41), PGE2 but not PGD2, F2 alpha, or I2 inhibited beta-EI release by about 60%. The concentrations of PGE2 in the incubation media, as measured by RIA, were somewhat higher than those of any other cyclooxygenase product (PGD2, F2 alpha, 6-keto-PGF1 alpha, thromboxane B2). Upon stimulation by AVP or CRF-(1-41), the concentrations of PGE2 increased, whereas those of PGD2 or F2 alpha remained unchanged. The release of beta-EI stimulated by high potassium concentration was not enhanced by indomethacin, although this release was sensitive to inhibition by PGE2. We conclude that PGE2 is formed locally subsequent to binding of the neurohormones and may act as a negative feedback-modulator of vasopressin's and CRF-(1-41)'s activity in the anterior pituitary gland.
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PMID:Adrenocorticotropin and beta-endorphin release from rat adenohypophysis in vitro: inhibition by prostaglandin E2 formed locally in response to vasopressin and corticotropin-releasing factor. 620 54

6-Ketoprostaglandin E1 effects on rat and rabbit renal adenylate cyclase-cyclic AMP systems were examined. Adenylate cyclase activity was assessed in the 1000 X g fractions prepared from different areas of kidney. 6-Ketoprostaglandin E1 caused a dose-dependent increase in rat cortical and medullary adenylate cyclase activity with 8 x 10(-6) M being the lowest effective concentration. Combinations of maximal stimulatory concentrations of 6-ketoprostaglandin E1 and prostaglandin I2 caused stimulation similar to that seen with either agent alone. In contrast, the combination of either prostaglandin with parathyroid hormone (cortex) or antidiuretic hormone (medulla) resulted in enzyme activity significantly greater than with either agent alone. Similar results were observed in the rabbit. In addition, rabbit cortical and medullary slice cyclic AMP content was increased by 6-ketoprostaglandin E1. Maximal stimulatory effects of 6-ketoprostaglandin E1 on adenylate cyclase activity and cyclic AMP content were similar to prostaglandin I2. Therefore, the similarity in physiologic actions of 6-ketoprostaglandin E1 and prostaglandin I2 may be due to the stimulation of adenylate cyclase by both agents. These prostaglandins and the polypeptide hormones appear to activate different renal adenylate cyclase-cyclic AMP systems.
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PMID:6-Ketoprostaglandin E1 stimulation of rat and rabbit renal adenylate cyclase-cyclic AMP systems. 626 Feb 31

Effects of prostaglandins (PG) on intracellular cAMP content were examined in an intact cell preparation of single nephron segments dissected from rat kidney. PGE2 markedly increased cell cAMP in the thin descending limb of Henle (tDL) in a dose-dependent manner. Significant increases in cell cAMP were observed at 1-10 ng/ml PGE2, concentrations prevailing in the renal medulla in vivo, and the increase reached a maximum at a PGE2 concentration of 10 micrograms/ml. PGI2 also increased cell cAMP in the tDL, but the doses required were two orders of magnitude higher than those for PGE2. PGF2 alpha had only a minor effect, if any. PGE2 but not PGI2 also increased cell cAMP of rabbit tDL, but to a lesser magnitude than that seen in the rat tDL. PGE2 increase cell cAMP slightly in the cortical-collecting tubules at 10 micrograms/ml but no significant effect was seen in other nephron segments tested including proximal convoluted tubules, cortical and medullary thick ascending limbs of Henle, and medullary-collecting tubules. Results suggest a possible physiological effect of PGE2 via cAMP on the tDL thereby affecting the function of the renal medulla. Such an effect of PGE2 may underlie, at least in part, in the inhibition by PGE2 of vasopressin-mediated urinary concentration.
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PMID:Effect of PGE2 on the cell cyclic AMP content in the thin descending limb of Henle of the rat. 633 May 12


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