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)

1. Experiments were carried out to test whether neosurugatoxin (NSTX) which blocks autonomic ganglia also acts centrally, like hexamethonium, on nicotinic cholinoceptors involved in the neural control of release of vasopressin and oxytocin from the neurohypophysis. 2. In the water-loaded rat under ethanol anaesthesia, nicotine 100 micrograms i.v. produced a pressor and an antidiuretic response accompanied by an increase in the urinary excretion of vasopressin and of oxytocin-like radioimmunoreactivity (OLRI). This indicates release of both vasopressin and oxytocin. 3. Under conditions in which tachyphylaxis was avoided, NSTX, 80 ng i.c.v., caused a prolonged inhibition of the release of both hormones by nicotine. 4. NSTX i.c.v. caused some reduction in the pressor response to nicotine. It is suggested that this response involves both central and peripheral stimulation of the sympathetic nervous system and that the central component is blocked by neosurugatoxin. 5. Muscarine, 40 ng i.c.v., produced a pressor and an antidiuretic response with increased urinary excretion of vasopressin and OLRI. All these effects were blocked by atropine but were not inhibited by NSTX. 6. Sodium nitroprusside (SN), 200 micrograms i.v., and hypertonic saline (HS; 1.54 M NaCl solution) 4 microliters i.c.v., both produced antidiuretic responses accompanied by increased urinary excretion of vasopressin and OLRI. The ratio of the excretion of vasopressin to that of OLRI was 5.1 +/- 1.3 (mean +/- s.e.: n = 8) for SN and 1.2 +/- 0.24 (mean +/- s.e.: n = 6) for HS.NSTX 80 ng i.c.v., caused a significant reduction in the antidiuretic response to the hypotension induced with SN: the increased urinary excretion of vasopressin was also significantly reduced but not that of OLRI. NSTX had no effect on the response to HS.7. We conclude that NSTX acts centrally on nicotinic cholinoceptors to block the release of vasopressin and oxytocin by nicotine and the release of vasopressin, but not that of oxytocin, by hypotension. It does not inhibit the release of either hormone by a central osmotic stimulus.
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PMID:The effect of neosurugatoxin on the release of neurohypophysial hormones by nicotine, hypotension and an osmotic stimulus in the rat. 150 51

The effects of phosphodiesterase inhibitors, an activator and an inhibitor of guanylyl cyclase, and cAMP and cGMP analogs on oxytocin-induced contractions have been studied in the testicular capsule of rats. The nonspecific phosphodiesterase inhibitors, theophylline and caffeine, attenuated the oxytocin-induced contractions via mechanisms that seem to be related to an increase in cAMP levels, since a similar effect was produced by dibutyryl cAMP. Sodium nitroprusside facilitated oxytocin-induced contractions. This effect was mimicked by dibutyryl cGMP. Methylene blue, an inhibitor of soluble guanylyl cyclase, decreased oxytocin-induced contractions, which suggests an involvement of guanylyl cyclase in the oxytocin effect. These results suggest that cAMP modulates the contraction and that cGMP, contrary to what happens in most smooth muscles, could participate in oxytocin-induced contractions in the testicular capsule of rats.
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PMID:Role of cyclic nucleotides in contraction induced by oxytocin in the testicular capsule of the rat in vitro. 899 Apr 88

Neurokinin A (NKA) is a tachykinin that participates in the control of neuroendocrine functions. The posterior pituitary lobe (PP) contains abundant nitric oxide synthase (NOS), suggesting that nitric oxide (NO) may play a role in controlling the release of neuropeptides and neurotransmitters. In the present project, we investigated the in vitro effect of NKA on oxytocin release from hypothalamic explants and PP of male rats and the possible involvement of NO in the action of NKA. Since NKA inhibits gamma-aminobutyric acid (GABA) release from PP, we also examined the role of NO in the effect of NKA on basal and K(+)-evoked GABA release. NKA (10(-7)-10(-5) M) significantly decreased oxytocin release from PP, whereas it did not affect its release from hypothalamic explants. The inhibitory effect of NKA on oxytocin release from PP was completely blocked by the NOS inhibitors N(G)-monomethyl-L-arginine (L-NMMA, 0.5 mM) or N(G)-nitro-L-arginine-methyl-ester (L-NAME, 1 mM). Sodium nitroprusside (0.5 mM), an NO releaser, had no effect on basal GABA release but significantly decreased K(+)-evoked GABA release. L-NMMA (0.3 mM) and L-NAME (0.5 mM) increased K(+)-evoked GABA release, indicating that NO plays an inhibitory role in GABA release from PP. The inhibition in both basal and K(+)-evoked GABA release induced by NKA (10(-7) M) was reduced by L-NAME (1 mM). Also, NKA (10(-7) M) increased NO synthesis as measured by [(14)C] citrulline production. Considered all together, our data indicate that NO may mediate the inhibitory effect of NKA on the release of both oxytocin and GABA from PP.
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PMID:Neurokinin A inhibits oxytocin and GABA release from the posterior pituitary by stimulating nitric oxide synthase. 1111 87

Magnocellular oxytocin neurons develop morphine dependence after intracerebroventricular infusion for 5 days as revealed by their profound excitation following naloxone-induced withdrawal. Oxytocin neurons strongly express nitric oxide synthase (NOS) and nitric oxide (NO) inhibits their activity. This study investigated whether excitation of oxytocin neurons during morphine withdrawal involves reduced activity of NOS and NO. Neuron activity was measured in urethane-anaesthetized rats with blood sampling for oxytocin radioimmunoassay and extracellular single unit firing rate recording of supraoptic nucleus oxytocin neurons. To compare morphine-dependent and -naive rats oxytocin secretion was measured during stimulation by intravenous hypertonic saline infusion. Prior treatment with Nomega-nitro-l-arginine methyl ester, a NOS inhibitor, facilitated osmotically stimulated oxytocin secretion in both morphine-dependent and -naive rats. The facilitation was not different between these groups when corrected for the slower responses observed in morphine-dependent rats. Treatment of morphine-dependent rats with Nomega-nitro-l-arginine methyl ester also enhanced oxytocin secretion during naloxone-precipitated withdrawal. Oxytocin neurons excited by withdrawal were recorded during microdialysis application to the supraoptic nucleus of the NO donor sodium nitroprusside alone and in combination with the GABAA antagonist bicuculline. Sodium nitroprusside inhibited oxytocin neurons during naloxone-precipitated morphine withdrawal and, while bicuculline alone increased firing rate, it did not reduce the inhibition by sodium nitroprusside, in contrast with previous findings in naive rats. Together, these findings indicate that NO restraint of oxytocin secretion is not curtailed during morphine dependence and remains a potent inhibitor of withdrawal excitation despite reduced effectiveness on GABA innervation of the supraoptic nucleus. Hence there is no evidence that changes in NO regulation underlie excitation of oxytocin neurons during opiate withdrawal in morphine dependence.
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PMID:The role of nitric oxide in morphine dependence and withdrawal excitation of rat oxytocin neurons. 1462 55

Oxytocin (OT) plays an important role in pain modulation and antinociception in the central nervous system. However, little is known about its peripheral effects. This study was conducted to investigate the effect of OT on the electrical properties of neurons in the dorsal root ganglia (DRG) and the underlying mechanisms. DRG neurons from adult rats were acutely dissociated and cultured. Intracellular Ca(2+) was determined by fluorescent microscopy using an indicator dye. The electrical properties of DRG neurons were tested by patch-clamp recording. The oxytocin receptor (OTR) and neuronal nitric oxide synthase (nNOS) on DRG neurons were assessed with immunofluorescence assays. OTR co-localized with nNOS in most of Isolectin B4 (IB4)-binding cultured DRG neurons in rats. OT decreased the excitability, increased the outward current, and evoked the membrane hyperpolarization in cultured DRG neurons. Sodium nitroprusside (SNP), the donor of nitric oxide (NO), exerted similar effects as OT on the membrane potential of cultured DRG neurons. OT increased the production of NO in DRGs and cultured DRG neurons. Pre-treatment of the OTR antagonist atosiban or the selective nNOS inhibitor N-Propyl-l-arginine (NPLA) significantly attenuated the hyperpolarization effect evoked by OT. OT produced a concentration-dependent increase in intracellular Ca(2+) in DRG neurons that responds to capsaicin, which can be attenuated by atosiban, but not by NPLA. OT-evoked membrane hyperpolarization and increase of outward current were distinctly attenuated by glibenclamide, a blocker of ATP-sensitive K(+) (KATP) channel. OT might be an endogenous antinociceptive agent and the peripheral antinociceptive effects of OT are mediated by activation of the Ca(2+)/nNOS/NO/KATP pathway in DRG neurons.
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PMID:Oxytocin-induced membrane hyperpolarization in pain-sensitive dorsal root ganglia neurons mediated by Ca(2+)/nNOS/NO/KATP pathway. 2561 53