Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01178 (oxytocin)
 15,767 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Oxytocin, bradykinin, melittin and A23187 increased cyclic GMP levels through activation of soluble guanylate cyclase in cultured porcine kidney epithelial cells, LLC-PK1. NG-monomethyl-L-arginine, an inhibitor of endothelium-derived relaxing factor/nitric oxide formation, decreased both basal and stimulated levels of cyclic GMP in a concentration-dependent manner. L-Arginine, but not D-arginine, augmented basal as well as stimulated levels of cyclic GMP and prevented the inhibition induced by NG-monomethyl-L-arginine. Similar effects of L-arginine were also observed with L-argininamide, L-arginine ethyl ester, L-arginine methyl ester and the dipeptide L-arginyl-L-aspartic acid. NG-monomethyl-L-arginine did not affect cyclic GMP accumulation induced by sodium nitroprusside, an activator of soluble guanylate cyclase, and atrial natriuretic factor, an activator of particulate guanylate cyclase. Stimulatory effects of oxytocin, glyceryl trinitrate, sodium nitroprusside, bradykinin, melittin and A23187 on cyclic GMP accumulation were enhanced with superoxide dismutase and diminished with oxyhemoglobin. However, atrial natriuretic factor-induced cyclic GMP accumulation was not affected. Furthermore, endothelium derived relaxing factor-like activity was detected in the conditioned medium from LLC-PK1 cells stimulated with oxytocin. Based on these data, we conclude that endothelium-derived relaxing factor is produced in this cell type and participates in the regulatory mechanism of cyclic GMP formation as an intra- and intercellular messenger for activation of soluble guanylate cyclase.
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PMID:Formation of endothelium-derived relaxing factor in porcine kidney epithelial LLC-PK1 cells: an intra- and intercellular messenger for activation of soluble guanylate cyclase. 167 Oct 98

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

Magnocellular hypothalamic neurons of the paraventricular (PVN) and supraoptic (SON) nuclei have been shown to contain a wide variety of messenger molecules in addition to vasopressin and oxytocin, including the nitric oxide (NO)-synthesizing enzyme (NOS). In this paper we have investigated the effects of salt loading on the expression of NOS by means of immunohistochemistry and in-situ hybridization. The results show an increase in the number of NOS-immunoreactive (IR) neurons both in the PVN and the SON after 5 and 14 days of salt loading. Several of these neurons were double labelled with vasopressin antiserum. In situ hybridization showed a marked increase in the number of neurons expressing NOS mRNA and a stronger signal in individual neurons. The present results suggest a role for NO in the magnocellular hypothalamic system after salt loading.
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PMID:Nitric oxide synthase increases in hypothalamic magnocellular neurons after salt loading in the rat. An immunohistochemical and in situ hybridization study. 751 26

I.c.v. administration of a nitric oxide (NO) synthase inhibitor (NG-monomethyl-L-arginine, NMMA, 500 micrograms/5 microliters) to conscious rats deprived of water for 24 h attenuated drinking and decreased glucose utilization in the subfornical organ and median preoptic nucleus. NMMA did not alter the enhanced glucose utilization in the hypothalamo-neurohypophysial system (HNS) of dehydrated rats, although it has been shown to increase, selectively, oxytocin (OT) secretion [18]. This suggests that NO may act in the neural lobe to inhibit OT secretion and promote the preferential release of vasopressin during dehydration. This effect is similar to the blockade of endogenous opiate receptors by naloxone.
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PMID:Central inhibition of nitric oxide synthase attenuates water intake but does not alter enhanced glucose utilization in the hypothalamo-neurohypophysial system of dehydrated rats. 752 94

In order to establish whether nitric oxide (NO) participates in the regulation of arginine-vasopressin (AVP) and/or oxytocin (OT) secretion in humans, six normal men were treated with placebo (normal saline) or the NO synthase inhibitor N,G-nitro-L-arginine methyl ester (L-NAME), given at doses (40 micrograms kg-1 injected plus 50 micrograms kg-1 infused i.v.) previously found to be unable to change blood pressure. Experiments were carried out both in basal conditions and during stimulation of posterior pituitary secretion with insulin (0.15 IU kg-1)-induced hypoglycaemia. The administration of saline or L-NAME alone was unable to change basal AVP or OT levels. Insulin-induced hypoglycaemia, however, enhanced plasma AVP and OT levels by two-fold in the absence of L-NAME and by four-fold in the presence of the NO synthase inhibitor (NOS). Blood glucose levels decreased in a similar manner during the insulin tolerance tests, regardless of L-NAME administration. In all experiments, AVP and OT responses to hypoglycaemia followed a similar pattern, with mean peak levels at 45 min. These data suggest that in normal men NO is not involved in regulation of basal AVP and OT secretions, whereas it exerts an inhibitory role in the control of the posterior pituitary hormone responses to hypoglycaemia.
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PMID:Inhibitory control of nitric oxide on the arginine-vasopressin and oxytocin response to hypoglycaemia in normal men. 753 64

The endothelins consist of a family of vasoconstrictor peptides originally isolated from endothelial tissue which are now known to be involved in neuroendocrine regulation. However, while there are data indicating the involvement of endothelins in the modulation of the hypothalamo-pituitary-adrenal (HPA) axis, the precise mechanisms involved have been unclear. We have therefore used a previously validated rat hypothalamic explant system in order to investigate the possible modulation of the neurohypophyseal hormones vasopressin and oxytocin, and corticotropin-releasing hormone (CRH), by endothelin-1 (ET-1) and endothelin-3 (ET-3). Following a period of stabilisation, the release of vasopressin, oxytocin and CRH remained approximately constant in successive 20-min incubations. Addition of ET-1 stimulated the release of vasopressin at a dose of 0.1 nmol/l (p < 0.05), and both vasopressin and oxytocin at 10 nmol/l (p < 0.01 and 0.05, respectively). The release of vasopressin and oxytocin induced by 10 nmol/l ET-1 were both totally blocked by co-incubation with either 1 or 10 mumol/l of the specific ETA receptor subtype antagonist cyclo (D-Trp-D-Asp-Pro-D-Val-Leu) (BQ-123). ET-1 had no effect on CRH release in the dose range of 0.1-1,000 nmol/l. In case any possible stimulation of CRH might be masked by simultaneous generation of nitric oxide (NO), an inhibitor of CRH secretion, addition of ET-1 was also carried out in the presence of the NO synthase inhibitor, L-NO-Arg: ET-1 was again without effect in this dose range.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Endothelin-1 stimulates the in vitro release of neurohypophyseal hormones, but not corticotropin-releasing hormone, via ETA receptors. 753 87

The purpose of our study was to examine the relaxant effects of sodium nitroprusside (SNP) and cyclic guanosine 3'-5'-monophosphate (cGMP) on pregnant rat myometrium. Using very thin muscle strips, which allows diffusional access of applied drugs (in a few seconds), contractile properties were examined. This technique facilitates study of SNP's effects on uterine contractility as nitric oxide is rapidly inactivated to NO2. SNP did not decrease the amplitudes of 45 mmol/l KCl contractions but decreased spontaneous contractions and 1 mumol/l carbachol contractions. The relaxation of carbachol contractions by SNP were antagonized by methylene blue. In addition, 8-bromo-cyclic guanosine monophosphate (8-bromo-cGMP) also inhibited KCl-, carbachol- and oxytocin-induced contractions, however, the relaxant effect of 8-bromo-cGMP was much greater on carbachol and oxytocin contractions than on KCl contractions. Cyclic GMP (1 microM) decreased contractions evoked by various concentrations of Ca2+ and carbachol with 1 mumol/l GTP-gamma S in skinned (membrane-permeable) strips. These results demonstrate that SNP stimulates guanylate cyclase to produce cGMP and that the relaxant effect of cGMP was predominant on pharmaco-mechanical coupling. The cyclic-GMP system may help in maintaining pregnancy and preventing uterine contractions during exposure to stimulating agonists.
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PMID:Relaxant effects of nitric oxide and cyclic GMP on pregnant rat uterine longitudinal smooth muscle. 764 71

Intracerebroventricular (i.c.v.) administration of NG-monomethyl-L-arginine monoacetate (NMMA; 500 micrograms; 402 mM) and NG-nitro-L-arginine methyl ester (NAME; 270 micrograms; 200 mM), inhibitors of nitric oxide synthase, enhanced the rise in oxytocin but not vasopressin levels in plasma of conscious rats following 24 h of water deprivation. This effect of NMMA occurred by 10 min after administration, reached its peak at 15 min and decreased by 20 min. Daily administration of lower doses (50 micrograms and 0.5 microgram/5 microliter, i.c.v.) of another inhibitor of nitric oxide synthase, NG-nitro-L-arginine, just before and after 24 h of water deprivation and in control animals treated similarly were without effect on either vasopressin or oxytocin levels. Nitric oxide, therefore, attenuates preferentially the release of oxytocin during dehydration.
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PMID:Central inhibition of nitric oxide synthase preferentially augments release of oxytocin during dehydration. 768 65

The effect of NG-nitro-L-arginine methyl ester and NG-monomethyl-L-arginine, two inhibitors of nitric oxide synthase, on apomorphine- and oxytocin-induced penile erection and yawning, was studied in male rats after intravenous and intracerebroventricular administration. Both compounds prevented dose-dependently apomorphine and oxytocin responses, when given systemically (5-50 mg/kg) or centrally (30-500 micrograms per rat), but NG-nitro-L-arginine methyl ester was about 5 times more potent than NG-monomethyl-L-arginine. The D-isomer of NG-monomethyl-L-arginine, which does not inhibit nitric oxide synthase, was ineffective. The results suggest that central nitric oxide is involved in the expression of penile erection and yawning induced by apomorphine and oxytocin.
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PMID:Nitric oxide synthase inhibitors prevent apomorphine- and oxytocin-induced penile erection and yawning in male rats. 768 37

In order to evaluate a possible role of brain nitric oxide (NO) on the control of penile erection, the effect of nitroglycerin, that is thought to act by producing NO, was studied on spontaneous penile erection in male rats. In addition the effect of drugs that prevent NO formation and/or activity such as NG-nitro-L-arginine methyl ester (NAME) and methylene blue, on N-methyl-D-aspartic acid (NMDA)-, apomorphine- and oxytocin-induced penile erection was also studied. Nitroglycerin induced penile erection in a dose-dependent manner when given intracerebroventricularly (i.c.v.) (33-99 micrograms) or in the paraventricular nucleus of the hypothalamus (0.8-3.3 micrograms). Nitroglycerin-induced penile erection was prevented by the guanylate cyclase inhibitor methylene blue injected i.c.v. (200-400 micrograms) but not in the paraventricular nucleus of the hypothalamus (10-20 micrograms). Conversely, NMDA-, apomorphine- and oxytocin-induced penile erection was prevented by NAME (150 micrograms) or methylene blue (400 micrograms) given i.c.v. NAME (20 micrograms), but not methylene blue (20 micrograms), was effective in preventing the behavioral response also when injected in the paraventricular nucleus. The present results suggest that NO is a common mediator of several neurotransmitters involved in the control of this primary male sexual function.
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PMID:Nitric oxide is a central mediator of penile erection. 787 Feb 89


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