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)

The effect of ischemia-reperfusion on endothelium-dependent relaxations and reactivity of vascular smooth-muscle cells was studied in rings of basilar arteries obtained from six dogs exposed to 12 min of complete global cerebral ischemia followed by 100 min of reperfusion. Three sham-operated control dogs served as controls. Ischemia was induced either by an increase in intracranial pressure or by aortic occlusion. The rings were suspended for isometric tension recording in physiological salt solution. Ischemia-reperfusion did not affect endothelium-dependent relaxations to vasopressin and bradykinin. In rings without endothelium relaxations to sodium nitroprusside, molsidomine (SIN-1), and papaverine as well as contractions to 5-hydroxytryptamine and KCl were preserved. These results demonstrate that in large canine cerebral arteries, ischemia-reperfusion of these durations does not affect relaxations mediated by activation of endothelium or direct relaxations and contractions of vascular smooth-muscle cells.
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PMID:Ischemia-reperfusion does not affect reactivity of isolated canine basilar artery. 187 14

The response to small peptides such as Arg-vasopressin, oxytocin and tachykinins was investigated in cultured porcine aortic endothelial cells. The production of endothelium-derived nitric oxide was assessed indirectly by the accumulation of cyclic GMP, a response that is due to the increased activity of soluble guanylate cyclase of the endothelial cells after release of the mediator. Arg-vasopressin, oxytocin, substance P and physalae-min (an analog of substance P, pGlu-Ala-Asp-Pro-Asn-Lys-Phe-Tyr-Gly-Leu-Met-NH2) markedly and transiently stimulated the production of cyclic GMP without affecting that of cyclic AMP. Treatment of endothelial cells with either hemoglobin or methylene blue reduced significantly both the basal and stimulated level of cyclic GMP. The production of cyclic GMP evoked by Arg-vasopressin and substance P was inhibited selectively by NG-monomethyl-L-arginine but not by its D-enantiomer. The neurohypophyseal hormones and related peptides stimulated the accumulation of cyclic GMP in a concentration-dependent manner, with the following relative order of potency: oxytocin greater than Lys-vasopressin greater than Arg-vasopressin much greater than [deamino-Cys1, D-Arg8]-vasopressin. The production of cyclic GMP evoked by oxytocin was inhibited selectively by [d(CH2)5, Tyr(OMe)2, Orn8]-vasotocin, an oxytocin antagonist. The production of cyclic GMP evoked by Arg-vasopressin and Lys-vasopressin was inhibited by [beta-mercapto-beta, beta-cyclopentamethylene-propionyl1, O-Me-Tyr2, Arg8]-vasopressin, a selective V1-receptor antagonist. The moderate production of cyclic GMP evoked by [deamino-Cys1, D-Arg8]-vasopressin was inhibited significantly by the V1-receptor antagonist. The peptide antagonists affected only minimally or not at all the production of cyclic GMP evoked by a donor of nitric oxide, SIN-1 (3-Morpholino-Sydnonimine). These observations indicate that 1) neurohypophyseal hormones and tachykinins stimulate the accumulation of cyclic GMP in cultured porcine aortic endothelial cells by increasing the production of endothelial-derived nitric oxide, which in turn enhances the activity of soluble guanylate cyclase; 2) the production of cyclic GMP in response to oxytocin is due to activation of oxytocinergic receptors; and 3) the production of cyclic GMP evoked by Arg-vasopressin and Lys-vasopressin is due mostly to activation of V1-vasopressinergic receptors.
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PMID:Neurohypophyseal peptides and tachykinins stimulate the production of cyclic GMP in cultured porcine aortic endothelial cells. 217 9

The present study aims at investigating the effect of pharmacological manipulation of nitric oxides (NOs) formation in the rat neurohypophysis on the secretion of vasopressin (AVP). We found that the NO synthase antagonist L-NAME and free-ferrous hemoglobin (an NO inactivator) produced a transient and significant enhancement of basal secretion of AVP from incubated glands. Conversely, the NO precursor L-arginine (but not its inactive counterpart D-arginine) antagonized the stimulatory influence of L-NAME on both AVP and oxytocin (OT) output. Elevation of NOs formation triggered by means of the NO donor SIN-1 likewise dampened spontaneous, as well as stimulated, AVP release. It is concluded that NOs molecules show up as potent regulators of neuropeptide secretion at the level of nerve terminals in the neurohypophysis.
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PMID:Evidence for an inhibitory effect of nitric oxides on neuropeptide secretion from isolated neural lobe of the rat pituitary gland. 751 25

The enzyme nitric oxide (NO) synthase is present in the paraventricular nucleus, while nitric oxide has recently been shown to inhibit the stimulated release of corticotrophin-releasing hormone (CRH) in vitro. Thus the possible role of NO in regulating, vasopressin (AVP), which also plays an important role in pituitary-adrenal activity, has been investigated. The effects were studied of the NO donors, L-arginine, syndnonimine-1 (SIN-1) and sodium nitroprusside, on both the basal and stimulated release of AVP, employing a previously validated system. Rat hypothalami were incubated in either medium alone or medium containing the test substances and hormone release was measured by RIA. The effect of L-arginine in the presence of the NO synthase inhibitor, L-NMMA, was also investigated. L-arginine reduced KCl-evoked AVP release; this effect was reversed by L-NMMA and reduced by the addition of ferrous human Hb. Similarly, SIN-1 and sodium nitroprusside attenuated KCl-evoked AVP release. L-arginine also reduced IL-1 beta-stimulated AVP release. NO appears to directly and specifically inhibit the stimulated release of AVP from rat hypothalamic explants in vitro, similar to its effects on CRH. These findings provide further evidence that NO may be involved in neuroendocrine regulation.
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PMID:Nitric oxide modulates the release of vasopressin from rat hypothalamic explants. 768 60

Experiments were designed to determine the role of the L-arginine pathway in endothelium-dependent relaxations to vasopressin. The effects of L-arginine analogues NG-nitro-L-arginine (L-NNA), NG-nitro-L-arginine methyl ester (L-NAME), and NG-monomethyl-L-arginine (L-NMMA) on basal and vasopressin-induced activity of nitric oxide synthase were studied in isolated canine basilar arteries. Rings with and without endothelium were suspended for isometric tension recording in Krebs-Ringer bicarbonate solution bubbled with 94% O2-6% CO2 (37 degrees C, pH 7.4). Radioimmunoassay was used to determine the level of guanosine 3',5'-cyclic monophosphate (cGMP). All experiments were performed in the presence of indomethacin, a cyclooxygenase inhibitor. L-NAME and L-NMMA caused endothelium-dependent contractions and inhibited basal production of cGMP. In contrast, L-NNA did not affect basal tone or basal production of cGMP. L-Arginine analogues inhibited relaxations to vasopressin but did not affect relaxations to a nitric oxide donor, molsidomine (SIN-1). The effects of L-NNA, L-NAME, and L-NMMA were reversed in the presence of L-arginine. The relaxations to vasopressin were associated with an increase of cGMP levels in the arterial wall. This effect of vasopressin was inhibited in the presence of L-NNA. These studies suggest that the relaxations to vasopressin are mediated by activation of the endothelial L-arginine pathway, leading to increased production of nitric oxide, with subsequent activation of guanylate cyclase in smooth muscle cells. In canine basilar artery, L-NAME and L-NMMA are nonselective inhibitors of both basal and stimulated production of nitric oxide, whereas L-NNA selectively inhibits vasopressin-induced activation of the L-arginine pathway.
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PMID:Endothelial L-arginine pathway and relaxations to vasopressin in canine basilar artery. 838 55

We investigated the effect of the intracerebroventricular injection of the nitric oxide (NO) donor 3-morpholino-sydnonimine (SIN-1) on the release of adrenocorticotropin hormone (ACTH) and the neuronal response of hypothalamic neurons responsible for this release. Rats that were administered SIN-1 showed significant elevations in plasma ACTH levels, a response that was virtually abolished by antibodies against corticotropin-releasing factor (CRF) and significantly blunted by vasopressin (VP) antiserum. SIN-1 also upregulated heteronuclear (hn) transcripts for CRF and VP and messenger RNA (mRNA) levels for the immediate early gene NGFI-B and for CRF receptor type 1 (CRF-R(1)) in the parvocellular portion of the paraventricular nucleus (PVN) of the hypothalamus. Blockade of prostaglandin synthesis with ibuprofen did not alter the ACTH or the PVN response to SIN-1. The central nucleus of the amygdala and the supraoptic nucleus, regions that are involved in autonomic adjustments to altered cardiovascular activity, also responded to SIN-1 with elevated NGFI-B mRNA levels. However, the only change in mean arterial blood pressure caused by this NO donor was a transient and modest increase. To our knowledge, this is the first demonstration that in the intact rat NO stimulates the activity of PVN neurons that control the hypothalamic-pituitary-adrenal axis. It must be noted, however, that our results do not allow us to determine whether this effect was direct or mediated through PVN afferents. This study should help resolve the controversy generated by the use of isolated brain tissues to investigate the net effect of NO on hypothalamic peptide production.
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PMID:Nitric oxide stimulates ACTH secretion and the transcription of the genes encoding for NGFI-B, corticotropin-releasing factor, corticotropin-releasing factor receptor type 1, and vasopressin in the hypothalamus of the intact rat. 1046 Feb 69

We previously showed that the intracerebroventricular injection of the nitric oxide (NO) donor 3-morpholino-sydnonimine (SIN-1) released adrenocorticotropic hormone (ACTH) and upregulated transcripts for corticotropin-releasing factor (CRF) and vasopressin in the paraventricular nucleus (PVN) of the rat hypothalamus. In the present work, we microinfused SIN-1 into the PVN itself, the amygdala, the hippocampus or the frontal cortex to identify the brain regions that modulate the influence of NO on the hypothalamic-pituitary-adrenal (HPA) axis. Microinfusion into the PVN, which contains most of the CRF and vasopressin neurones that control HPA axis activity, significantly released ACTH. Microinfusion into the amygdala or the hippocampus, areas which also regulate HPA axis activity, similarly increased plasma ACTH levels. However, these responses were smaller and showed a delayed onset, compared to that observed following PVN treatment. In contrast, microinfusion of SIN-1 into the frontal cortex, which is not believed to exert a major direct influence on the HPA axis, was without effect. The observation that compared to microinfusion into the PVN, peak ACTH levels were both smaller and delayed when SIN-1 was microinfused into the amygdala or the hippocampus, and that SIN-1 only increased NO levels when injected into the PVN, suggests that the NO donor injected outside the PVN activates this nucleus by targeting pathways that connect it to these other regions rather than by leakage. Collectively, our results provide important clues regarding the putative role of these regions in modulating the influence of NO on the HPA axis.
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PMID:Microinfusion of a nitric oxide donor in discrete brain regions activates the hypothalamic-pituitary-adrenal axis. 1173 50

We investigated the ability of the nitric oxide (NO) donor 3-morpholino-sydnonimine (SIN-1) to release adrenocorticotropic hormone (ACTH) and up-regulate hypothalamic neurones following its intravenous (i.v.) injection. i.v. SIN-1 (0.2-1.8 mg/kg) produced dose-related increases in plasma ACTH levels which were blocked by prior neutralization of endogenous corticotropin-releasing factor (CRF) but not by vasopressin antibodies. In contrast, the intracerebroventricular (i.c.v.) injection of 50-microg SIN-1 released significantly larger amounts of ACTH, a response blunted by either CRF or vasopressin antibodies. While i.c.v. SIN-1 markedly up-regulated transcripts of the immediate early gene NGFI-B in the paraventricular nucleus (PVN) of the hypothalamus, no such response was observed following the i.v. injection of up to 2.0 mg/kg SIN-1. Finally, we found no evidence that the influence of the peripheral administration of SIN-1 on ACTH secretion is mediated by altered pituitary responsiveness to CRF or vasopressin. The fact that NO has a profound hypotensive influence in the periphery suggests that it may have released ACTH through this mechanism, although the absence of PVN neuronal response in regions that are activated by decreased blood pressure casts some doubt on this hypothesis. As the systemic injection of arginine derivatives that block NOS activity potently augment the ACTH response to circulating pro-inflammatory cytokines or vasopressin, the present findings indicate that the mechanisms responsible for this phenomenon are distinct from those responsible for ACTH released by i.v. SIN-1.
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PMID:Comparison between the influence of the intravenous and intracerebroventricular injection of a nitric oxide donor on adrenocorticotropic hormone release and hypothalamic neuronal activity. 1212 94

Nitric oxide (NO) and carbon monoxide (CO) are endogenously synthesized gaseous molecules that act as neurotransmitters in central nervous system. In this study we investigated the modulatory role of NO and CO in lipopolysaccharide (LPS)-induced vasopressin and oxytocin secretion. Intracerebroventricular (i.c.v.) injection of N omega-L-nitro-arginine methyl ester (L-NAME), 3-morpholino-sydnonimine (SIN-1), zinc deuteroporphyrin 2,4-bis glicol (ZnDPBG) or hemin did not change the basal vasopressin and oxytocin plasma levels. After endovenous LPS administration, plasma vasopressin and oxytocin increased, reaching a peak at 60 min, and returning to basal levels afterwards. LPS administration induced a higher vasopressin and oxytocin plasma levels in rats previously treated with L-NAME and ZnDPBG (P<0.05) compared to rats pre-treated with vehicle. On the other hand, in rats previously treated with SIN-1 or hemin, there was a significant reduction in the vasopressin and oxytocin secretion. These findings confirm the inhibitory role of NO and CO in the LPS-induced vasopressin and oxytocin secretion.
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PMID:Inhibitory effect of gaseous neuromodulators in vasopressin and oxytocin release induced by endotoxin in rats. 1589 92

The presence of nitric oxide synthase (NOS), the enzyme that catalyses the formation of nitric oxide (NO), in the circumventricular organs and magnocellular neurones suggests an important role of NO in the modulation of vasopressin (AVP) and oxytocin (OT) release. Intracerebroventricular (I.C.V.) injection of angiotensin II (Ang II) stimulates the release of AVP, OT and atrial natriuretic peptide (ANP), with the resultant antidiuretic and natriuretic effects. This study investigated the interaction between nitrergic and angiotensinergic pathways on the release of AVP, OT and ANP and on urinary volume and sodium excretion in water-loaded rats. Unanaesthetized, freely moving, male Wistar rats received two water loads followed by an injection into the lateral ventricle of an inhibitor of NOS (L-NAME), a NO donor [3-morpholinylsydnoneimine chloride (SIN-1) or S-nitroso-N-acetyl penicillamine (SNAP)] or vehicle (isotonic saline) and, 20 min after, they received a second I.C.V. injection of Ang II or vehicle. Injections of L-NAME or Ang II produced an increase in plasma levels of AVP, OT and ANP, a reduction in urinary volume and an increase in sodium excretion. Pretreatment with L-NAME enhanced the Ang II-induced increase in AVP, OT and ANP release, as well as the antidiuresis and natriuresis. Injection of SIN-1 or SNAP did not modify hormonal plasma levels and urinary parameters. In contrast SNAP blocked the AVP, OT and ANP release, as well as antidiuretic and natriuretic responses induced by ANG-II. Thus, the central nitrergic system can act to inhibit AVP, OT and ANP secretion and the antidiuretic and natriuretic effects in response to Ang II.
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PMID:Central nitric oxide blocks vasopressin, oxytocin and atrial natriuretic peptide release and antidiuretic and natriuretic responses induced by central angiotensin II in conscious rats. 1751 44


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