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Query: UNIPROT:P01178 (oxytocin)
 15,767 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Against the background of renewed interest in the existence of reflex ovulation in many animal species and the possibility of its existence in man, this review on current research efforts embraces the multitude of nervous influences and stimuli accompanying cohabitation. Species showing reflex ovulation are not restricted to those using this as the sole ovulatory mechanism, but include also so-called facultative ovulators, which seem to use this mechanism as a last resort to assure reproductive capacity under adverse situations (rat); and species which for the length of the standing heat period become temporarily induced ovulators for the optimal coordination of all necessary steps to assure fertility (cattle, pig, sheep); and species in which frequent cohabitation (rat) or a single coitus after artificial insemination (sheep) assures either optimal ovulation or conception rates. Copulation might not always be essential; some of the cohabitation-related reflexes might be transmitted by olfactory, ocular, tactile and acoustic stimuli; emotions may play a role. These stimuli are transmitted to the CNS from the periphery by afferent nervous pathways, and are translated in the thalamic-hypothalamic-pituitary complex into neurohormonal phenomena, causing ovulation; or may cause, mainly by LH and/or oxytocin discharge, an acceleration or augmentation of processes involved in spontaneous ovulation. Intensive biochemical and pharmacological studies have unveiled some of the neurohormonal mechanisms involved in the hypothalamus and how these stimuli are transmitted to the pituitary or received at the ovarian level, as hormonal or neurohormonal phenomena.
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PMID:Current research in coitus-induced ovulation: a review. 81 May 83

Calcium antagonists are valuable pharmacological tools for the study of stimulussecretion and excitation-contraction coupling mechanisms. Two 2-substituted 3-dimethylamino-5,6-methylenedioxyindene hydrochlorides were tested for antagonism of the spasmogenic action of various agonists on isolated smooth muscle preparations. The 2-n-propyl and 2-n-butyl aminoindenes (5 X 10(-5) to 10(-4) M) blocked the spasmogenic action on the estrogen-treated rat uterus of prostaglandin E2 (10(-7) M), prostaglandin F2alpha tromethamine salt (10(-7) M), oxytocin (10(-3) U/ml), barium chloride (BaCl2-2H2O; 2.2 X 10(-4) M), acetylcholine chloride (10(-6) M) and ergonovine maleate (7.5 X 10(-4) M); they also blocked the contractile effect on the ileum of acetylcholine chloride (10(-6) M; rat) and histamine hydrochloride (10(-6) M; guinea pig). In further experiments on rat uterus using the agonists acetylcholine chloride (10(-6) M; which presumably acts by increasing influx of extracellular calcium into cells) and barium chloride (2.2 X 10(-4) M; which presumably contracts smooth muscle by releasing intracellular calcium), a progressive increase in extracellular calcium concentration (from 9 X 10(-4) to 7.2 X 10(-3) M CaCl2-2H2O) was paralleled by progressive reversal of the blockade produced by both 2-substituted aminoindene antagonists. In studies on the perfused bovine adrenal medulla, the 2-n-propyl aminoindene (10(-4) M) completely blocked the calcium-dependent catecholamine secretion evoked by 0.1 and 3.3 mM carbachol, without affecting the calcium-independent catecholamine secretion evoked by 33 mM acetaldehyde. These findings suggest that the aminoindene antagonists interfere with the action of calcium and that in smooth muscle the antagonism is at an intracellular site involved in excitation-contraction coupling.
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PMID:Pharmacological evaluation of new calcium antagonists: 2-substituted 3-dimethylamino-5,6-methylenedioxyindenes. 85 Jan 35

In urethane-anaesthetized ovariectomized rats, injection of porcine relaxin (7.5 and 15 micrograms/kg, i.v.) caused a sustained increase in circulating plasma oxytocin and vasopressin concentrations; 10 micrograms relaxin/rat i.v. produced a smaller but significant increase in plasma oxytocin concentration in conscious ovariectomized rats. A significant increase in oxytocin concentration and inhibition of the spontaneous milk-ejection reflex was also seen in anaesthetized (ovary intact) lactating rats following injection of relaxin (7.5 micrograms/kg, i.v.). To investigate whether relaxin acts by increasing the electrical activity of oxytocin neurones or by facilitating stimulus-secretion coupling in the pituitary, the electrical activity of neurones in the supraoptic nucleus was recorded in urethane-anaesthetized lactating rats and in ovariectomized rats. Porcine relaxin (10 micrograms/rat, i.v.) increased the firing rate of both oxytocin and vasopressin neurones in the supraoptic nucleus in lactating rats. The response to relaxin was unaffected by subsequent injection of naloxone (1 mg/kg, i.v.). Oxytocin neurones were also activated by injection of relaxin (10 micrograms/rat) into ovariectomized rats. Combining the electrophysiological data, the neuronal activation following relaxin was significantly correlated with the level of spontaneous activity prior to relaxin injection. The results show that relaxin acts centrally to increase circulating plasma oxytocin and vasopressin concentrations by an opioid-independent mechanism.
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PMID:Relaxin increases the firing rate of supraoptic neurones and increases oxytocin secretion in the rat. 173 54

The action of acute administration of oxytocin (OXY), vasopressin (AVP) or its analog 1-deamino-8-D-arginine-vasopressin (dDAVP) on basal and stress induced PRL release in normal male rats and the effect of chronic injection of AVP on PRL stress response in AVP deficient rats were studied. The hormones (OXY, 600 ng min-1 per rat; AVP 6, 12 or 24 ng min-1 per rat and dDAVP 24 ng min-1 per rat) were infused to conscious rats via the jugular vein for 10 min and then the rats were immobilized under continuing the infusion for further 20 min. In parallel experiments arterial blood pressure (BP) was measured. OXY and 24 ng min-1 AVP caused high BP elevation of the same magnitude, yet the effect of 12 ng min-1 AVP was significantly lower. Neither OXY, dDAVP, nor 6 and 12 ng min-1 of AVP affected basal or stress stimulated PRL values when compared with saline treated animals. 24 ng min-1 of AVP highly stimulated nonstressed PRL levels and no additional stress effect was observed. Intramuscular injection of 2 micrograms (1 U) of AVP daily for 7 days did not influence the basal values or stress induced PRL response in Brattleboro homogygous rats as compared with vehicle treated controls or heterozygous rats treated with AVP or vehicle. These results show that the infusion of 24 ng min-1 per rat of AVP stimulated PRL release which cannot be explained by the nonspecific effect of high BP. Repeated AVP administration did not modulate either the basal or IMO stress stimulated PRL secretion in rats with or without genetic vasopressin deficiency.
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PMID:Do the circulating neurohypophysial hormones affect basal or stress induced prolactin (PRL) release in male rats? 176 5

Increasing evidence indirectly suggests a role for oxytocinergic neurons in the control of ingestive behaviors. The present study was aimed at directly investigating a possible effect of oxytocin on food and water intake in rats. Oxytocin, whether administered intracerebroventricularly (ICV) (1-10 micrograms/rat) or intraperitoneally (IP) (375-3,000 micrograms/kg) dose dependently inhibited food intake in freely feeding animals; in schedule-fed animals fasting for 21 h, oxytocin not only reduced food intake but also reduced the time spent eating and increased the latency to first meal. On the other hand, oxytocin antagonist d(CH2)5Tyr(Me)-[Orn8]-vasotocin, ICV injected at the dose of 10 micrograms/rat, increased food intake and time spent eating and reduced the latency to first meal; moreover, it completely prevented the effect of oxytocin. Water intake was studied both in freely drinking animals and in three different models of thirst (water deprivation, hypertonic saline administration, angiotensin II injection). In all cases, oxytocin dose dependently inhibited water intake, in a dose range of 0.1-10 micrograms/rat (ICV) or 93-750 micrograms/kg (IP). In the water deprivation model, ICV pretreatment with d(CH2)5Tyr(Me)-[Orn8]-vasotocin completely prevented the antidipsogenic effect of oxytocin. In conclusion, these data show that oxytocin directly inhibits food and water intake in rats, the effect being specifically mediated by brain oxytocin receptors. This may support the idea that the brain oxytocinergic system plays an important role in the regulation of ingestive behaviors.
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PMID:Oxytocin inhibits food and fluid intake in rats. 208 13

The roles of oxytocin and vasopressin on prolactin secretion were studied. Adult female Sprague-Dawley rats ovariectomized for two weeks and treated with a long-acting estrogen, polyestradiol phosphate for one week were used. Hormone administration and serial blood sampling were accomplished through indwelling intra-atrial catheters which were implanted two days before the experiment. Both oxytocin (20 micrograms/rat) and vasopressin (5 micrograms/rat) stimulated prolactin secretion within 10 min after injection and the effects were diminished by 30 min. In animals pretreated with a small dose of dopamine antagonist, sulpiride (1 microgram/rat), the effect of TRH on prolactin secretion was repeatedly shown to be potentiated. Same pretreatments with two different time intervals (30 and 60 min) between sulpiride and oxytocin/vasopressin administration, however, had no effect on oxytocin- or vasopressin-stimulated prolactin secretion. A vasopressin analog, 1-deamino-[D-Arg8]-vasopressin (dDAVP), with antidiuretic but no vasopressor activity was also used in the study. It was found that unlike vasopressin, dDAVP had no effect on prolactin secretion. In conclusion, both oxytocin and vasopressin can have a stimulatory effect on prolactin secretion when given in vivo. Unlike TRH, however, the action of oxytocin or vasopressin was not augmented by pretreatments of dopamine antagonist. The action of vasopressin on prolactin secretion may be a side effect of its vasopressor activity.
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PMID:Dopamine antagonism does not potentiate the effects of oxytocin and vasopressin on prolactin secretion. 226 68

Monoclonal antibodies (MAbs) raised against the neurophysin (NP) specifically synthesized with vasopressin (VP, VP-NP) were injected into the paraventricular nucleus (PVN) of the rat hypothalamus. Their fate was studied by immunocytochemistry from 1 min to 3 h after the end of injection. It could be demonstrated that the VP-NP MAbs penetrated in vivo into some magnocellular neurons of the injected PVN and were transported ipsi- and contralaterally in individual neurons and in accessory magnocellular groups. When the time after injection was longer than 15 min, the VP-NP MAbs were also carried in the fibers of the median eminence. The prior treatment of rats with colchicine did not prevent the uptake of VP-NP MAb in the neurons but inhibited the transport towards the eminential fibers, the individual neurons and accessory groups. The detection of the PVN endogenous peptides (VP and oxytocin) on the same brain sections indicates that the neuronal uptake was specific. It only occurred in the neurons which synthesized VP and never appeared in the brain of rats suffering from a genetic defect of the central VP synthesis (Brattleboro rat). These data support the hypothesis of the location on the cell surface of the VP-NP precursor in magnocellular neurons which synthesize VP. This membrane signal identifies the neuron and allows the immunological recognition of the neurosecretory neurons in vivo.
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PMID:Vasopressin neuron is the target of monoclonal antibodies raised against vasopressin-neurophysin injected in vivo. 265 73

We investigated whether a sustained increase in oxytocin secretion, with or without enhanced electrical activity of the cell-bodies of oxytocin neurones, leads to a rapid increase in oxytocin mRNA content in these neurones. To stimulate oxytocin release, naloxone (2.5 mg/kg i.v. twice, 30 min apart) was given to urethane-anaesthetized female rats after intracerebroventricular (i.c.v.) morphine or vehicle infusion for 5 days; in the latter, naloxone acts on the neurohypophysis to increase oxytocin release without affecting the electrical activity of oxytocin neurone cell-bodies, but in the former, naloxone acts both on the neucohypophysis and on the cell-bodies to excite them electrically. Oxytocin content in peripheral plasma was measured intermittently by radioimmunoassay for 4 h after i.v. naloxone or vehicle, then the brain was removed and cryostat sections were cut through the supraoptic nucleus (SON). Oxytocin mRNA content in individual neurones (25-50 per rat) was measured semiquantitatively by in situ hybridisation histochemistry, using a tritiated synthetic cDNA 25-mer oligonucleotide probe, autoradiographical visualisation, and computer-assisted image-analysis to measure silver grain density. Nalaxone increased oxytocin content in plasma 7-fold for at least 40 min in i.c.v. vehicle-infused rats, and 40-fold for at least 40 min in i.c.v. morphine-infused rats. Naloxone had no significant effect on the oxytocin mRNA content in labelled cells in the SON, and no effect on the proportion of labelled cells, in either the i.c.v. morphine- or i.c.v. vehicle-infused rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Does acute, intense stimulation of oxytocin neurones in the supraoptic nucleus increase their content of oxytocin mRNA? 274 58

Oxytocin, whether administered intraperitoneally (IP) (375-6,000 micrograms/kg) or intracerebroventricularly (ICV) (1-10 micrograms/rat), dose-dependently reduced food consumption and time spent eating and increased the latency to the first meal in rats fasted for 21 hr. Pretreatment with the oxytocin antagonist d(CH2)5Tyr(Me)-[Orn8]vasotocin (ICV 10 micrograms/rat) completely prevented the feeding inhibitory effect of an equal dose of ICV oxytocin, and per se increased food intake. Our data further support the hypothesis that oxytocin plays the role of neurotransmitter or neuromodulator in the CNS, and suggest that its involvement in a number of homeostatic systems may include appetite control.
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PMID:Influence of oxytocin on feeding behavior in the rat. 274 28

The role of oxytocin in male copulatory performance was reexamined in rats. Adult male rats were trained seven times for copulatory behavior, at weekly intervals. Oxytocin, either intraperitoneally injected (200 ng/rat) or intracerebroventricularly infused (1 ng/rat in 4 microliter saline) 60 and 5 min, respectively, before the eighth test, significantly shortened both the ejaculation latency and the postejaculatory interval. The intracerebroventricular infusion of saline alone (4 microliter/rat) had no effect at all.
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PMID:Oxytocin improves male copulatory performance in rats. 298 3


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