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

The neurones in the supraoptic and paraventricular nuclei (SON and PVN) which secrete vasopressin are separate from those which secrete oxytocin and are distributed in different parts of the nuclei. They may be distinguished electrophysiologically by a characteristic phasic pattern of firing. A selective afferent neural input to these neurones would provide a mechanism for the release of vasopressin independently of oxytocin in response to appropriate physiological stimuli. Release of vasopressin is controlled by changes in blood volume or pressure ('volume control') and in plasma osmolality ('osmotic control'). Stimuli involved in volume control such as haemorrhage, hypotension and carotid occlusion cause vasopressin to be released into the circulation with little or no detectable oxytocin. An osmotic stimulus releases vasopressin alone in some species but not apparently in the rat in which both hormones are released. Volume control is mediated reflexly by peripheral receptors in the cardiovascular system. Activation of baro- and stretch receptors results in inhibition, and activation of chemoreceptors in stimulation, of release. Afferent impulses from these receptors are conveyed in the vagi and carotid sinus nerves to the NTS on the dorsal surface of the brain stem. All afferent impulses to the NTS are excitatory. It follows that the afferents from chemoreceptors must stimulate an excitatory, and those from baro- and stretch receptors an inhibitory, projection from the NTS to the vasopressin-secreting cells in the SON and PVN. Two alternative models are presented of the neural pathways and transmitters involved. The model of Fig. 2 shows an excitatory relay through a cholinoceptive area on the ventral surface of the brain stem which has been termed the 'nicotine-sensitive area' because topical application of nicotine to this area in the cat released vasopressin without oxytocin. An inhibitory relay is shown through the A1 group of noradrenergic neurones on the ventral surface which selectively innervate the vasopressin-secreting neurones in the SON. This model implies an inhibitory role for noradrenaline acting on beta- or alpha 2-receptors. However the most recent investigations suggest an excitatory, rather than inhibitory, function of the A1 noradrenergic neurones involving alpha 1-receptors. This is the basis of the model in Fig. 3. The A1 neurones project either directly to the SON and PVN or indirectly through the lateral preoptic nucleus which lies in close proximity to the SON. The nicotine-sensitive area may be coincident with the A1 group of noradrenergic neurones.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Control of release of vasopressin by neuroendocrine reflexes. 290 66

Norepinephrine and the alpha-agonist phenylephrine in concentrations of 10(-5) to 10(-3) M prompted the release of radioimmunoassayable vasopressin (up to 150 pg/min) and oxytocin (up to 20 pg/min) from intraarterially perfused explants of rat basal forebrain. Drug effects were markedly reduced or abolished in the presence of the non-specific alpha-antagonists phentolamine and phenoxybenzamine, and the specific alpha 1-antagonist prazosin. In concert with recent in vivo and in vitro electrophysiological observations, these data imply that endogenous noradrenergic pathways to magnocellular neurosecretory cells are excitatory, mediated through activation of their alpha 1-receptors, thereby enhancing the release of both vasopressin and oxytocin in the neurohypophysis.
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PMID:Alpha 1-adrenergic receptor activation releases vasopressin and oxytocin from perfused rat hypothalamic explants. 301 17

A comparison was made of contractions produced by submaximal doses of oxytocin, noradrenaline, PGE2 and PGF2 alpha in estrogen-dominated rat uterus after the preparation had been loaded in Ca-free medium supplemented with EDTA 3 mM. The experiments were carried out in the presence of EDTA 1 mM to complex the contaminating Ca. The contraction was sustained as long as the preparation was exposed to the drug and was relaxed by washing. Cumulative concentration-response curves to oxytocin (6.25-100 microM), noradrenaline (0.05-1.6 mM), PGE2 (0.1-1.6 microM) and PGF2 alpha (0.02-0.32 microM) were made. The threshold concentration for PGF2 alpha was much lower than for PGE2, oxytocin and noradrenaline. Isoprenaline (10- -10(-4)M), KCl (56.3 mM) and caffeine (5 mM) were added. The results showed that isoprenaline and KCl did not produce contractile response. Caffeine produces only a small decrease in the resting tension and this effect is not reversible. After addition of noradrenaline, a concentration of oxytocin (6 microM) produced a uterine contraction smaller than the control response of uterus to oxytocin. The response to the oxytocin applied after washing out the caffeine was the same as the control response. All agonists tested that were capable of inducing uterine contraction in Ca-free medium act through specific receptors. This suggests a relation between receptor-operated Ca-channels and intracellular Ca-stores.
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PMID:Role of intracellular calcium stores in the contractile response of uterus to several agonists. 310 89

We have investigated the role of ascending noradrenergic pathways in the control of oxytocin (OT) and arginine-vasopressin (AVP) secretion during acute immobilization stress in male and female rats. 6-Hydroxydopamine-induced lesions of the ventral noradrenergic bundle (VNAB) resulted in a selective depletion of hypothalamic noradrenaline content. In sham-lesioned rats plasma levels of OT were raised following stress, the response being significantly greater in female compared with male animals. VNAB lesions were not associated with altered responses in female rats, whereas lesioned males exhibited markedly elevated OT stress responses. AVP secretion was not modulated in VNAB-lesioned rats of either sex. The results provide functional evidence of a sexually dimorphic inhibitory role of the VNAB in the control of OT secretion.
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PMID:Modulation of oxytocin secretion by ascending noradrenergic pathways: sexual dimorphism in rats. 310 13

The changes in plasma levels of arginine-vasopressin (AVP) and oxytocin (OXT) of rabbits by intraventricular administration of various drugs and their effects on the release of both hormones from the isolated posterior pituitary of rats were examined. An intraventricular injection of hypertonic saline, carbachol, angiotensin II, prostaglandin E2 or histamine to a rabbit increased the concentrations of plasma AVP and OXT, whereas serotonin decreased their plasma levels. Noradrenaline increased the concentration of OXT, but not that of AVP. Dopamine did not significantly affect the plasma level of either hormone. The release of AVP and OXT from the posterior pituitary fragments of rats was stimulated by changing the osmolality of the perfusion medium in vitro. Perfusion with medium containing dopamine suppressed the release of both hormones. However, the other bioactive amines and the drugs mentioned above did not affect the release of AVP and OXT.
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PMID:A study on the release mechanism of vasopressin and oxytocin. 323 19

The effects of acetylcholine, arginine vasopressin (AVP) and oxytocin (OXT) on both catecholamine and steroid secretion have been investigated using the isolated rat adrenal gland perfused in situ. Significant stimulation of steroid (aldosterone and corticosterone) secretion occurred with 1 mumol/l acetylcholine; the ED50 was approximately 20-fold higher (circa 20 mumol/l) than that for catecholamine secretion. The highest concentration of acetylcholine used (100 mumol/l) stimulated aldosterone secretion eight-fold; corticosterone secretion four-fold; noradrenaline and adrenaline secretion three-fold. AVP at 100 nmol/l but not at 1 nmol/l significantly stimulated the secretion of both steroids and catecholamines. OXT had no significant effect on corticosteroid or catecholamine secretion at either concentration. The effects on aldosterone secretion of simultaneous administration of acetylcholine and AVP were additive. No similar effect was seen on corticosterone or catecholamine secretion where the degree of stimulation was the same as for acetylcholine alone. OXT (100 nmol/l) inhibited acetylcholine-stimulated aldosterone secretion but had no effect on acetylcholine-stimulated catecholamine secretion. Carbachol was equipotent with acetylcholine in stimulating steroid secretion from the perfused gland. Our results support the hypothesis that acetylcholine may play a role in the control of steroid secretion by the rat adrenal cortex. They fail to support a role for AVP and OXT in modulating catecholamine secretion by the adrenal medulla except at high concentrations.
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PMID:Effect of arginine vasopressin and oxytocin on acetylcholine-stimulation of corticosteroid and catecholamine secretion from the rat adrenal gland perfused in situ. 323 22

Opioids intrinsic to the neurohypophysis inhibit secretion from magnocellular neurosecretory terminals. This study examined whether the actions of opioids are mediated via interactions with neurohypophysial catecholamine systems. Blocking the action of intrinsic opioids in the isolated neurohypophysis with naloxone enhanced evoked secretion of oxytocin (OXT) by 150% and of vasopressin (AVP) by 30%. The enhancement of OXT secretion was not significantly altered in neurohypophyses depleted of greater than 90% of noradrenaline content by prior lesion of the ventral noradrenergic tract, or depleted of greater than 90% of both noradrenaline and dopamine content by prior reserpine treatment. Significant enhancement of AVP secretion by naloxone did not occur following depletion of catecholamines. The data suggest: (1) the majority of the influence of intrinsic opioids on secretion of OXT is not mediated via interaction with noradrenaline or dopamine systems, (2) the weaker influence of intrinsic opioids over AVP secretion may be mediated via catecholamines, (3) the majority of neurohypophysial noradrenaline is derived from projections of ascending medullary cell groups.
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PMID:Opioid inhibition of secretion from oxytocin and vasopressin nerve terminals following selective depletion of neurohypophysial catecholamines. 324 53

Intracranial dialysis was used to measure the release of oxytocin (OXY), monoamines and their metabolites and uric acid (UA) from the substantia nigra (SN) and olfactory bulb (OB) of sheep during parturition, suckling, separation from lambs and eating. Results showed that OXY concentrations increased significantly during parturition, suckling and eating in the SN and during parturition and suckling in the OB. Concentrations of dopamine (DA) increased significantly in the SN during suckling and eating and in the OB during parturition and suckling. The dopamine metabolite, homovanillic acid, also increased significantly in the SN during parturition. Concentrations of the noradrenaline metabolite, 4-hydroxy-3-methoxyphenylethan-1,2-diol (MHPG) and the purine metabolite, UA, were significantly raised during parturition, suckling and separation from the lambs in the SN and increased UA levels were also found during eating. In a separate experiment it was confirmed that OXY was detectable in homogenates of both the SN and the OB. These results show that, in the sheep, OXY and DA release in the SN is associated with maternal and ingestive behaviour whereas similar release in the OB may only be related to maternal behaviour. Release of MHPG in the SN may be associated with maternal behaviour and/or stress.
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PMID:Intracranial dialysis measurement of oxytocin, monoamine and uric acid release from the olfactory bulb and substantia nigra of sheep during parturition, suckling, separation from lambs and eating. 335 76

To investigate the functions of the paraventricular nucleus (PVN) which plays an important role as an integration site for the neuroendocrine and autonomic nervous systems, the firing activity of PVN neurons was recorded from hypothalamic slice preparations during thermal, osmotic and chemical stimulation. Neurons responded to environmental factors such as temperature and osmolarity and both warm-responsive and cold-responsive neurons were observed in the PVN. Some PVN neurons were also osmoresponsive and unlike neurons in the supraoptic nucleus, most osmoresponsive PVN neurons decreased their firing rate during hyperosmotic stimulation. One of the classical transmitters, noradrenaline, exerted excitatory effects on PVN neurons through alpha 1- and beta-receptors and inhibitory responses through alpha 2-receptors. Atrial natriuretic polypeptide exerted inhibitory effects on putative parvocellular PVN neurons but it had no effect on putative magnocellular PVN neurons. An endogenous sugar derivative, 2-deoxytetronic acid, thought to be an endogenous satiety factor, elicited inhibitory effects, supporting the possibility that the PVN also may be related to feeding behaviour. Arginine-vasopressin and oxytocin which are synthesised in the magnocellular neurosecretory cells excited PVN neurons, suggesting that the PVN may have short circuits modulating neural activity within the nucleus itself. We conclude that neurons in the PVN may receive multiple information and act as one of the important integrative sites in the brain.
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PMID:Thermal, osmotic and chemical modulation of neural activity in the paraventricular nucleus: in vitro studies. 340 58

Two doses (0.3 and 3 ng peptide/animal) of oxytocin (OXT) and lysine-8-vasopressin (LVP) were earlier found to inhibit the development of tolerance to the hypothermic effect of ethanol in mice upon icv. administration. In the present paper the possible central monoaminergic correlates of the behavioral data were investigated. In tolerant animals the steady-state level of noradrenaline (NA) was increased in the hypothalamus, as was that of dopamine (DA) in the medulla oblongata; the serotonin (5-HT) and DA levels were decreased in the striatum as compared to those in the non-tolerant control. In the peptide-pretreated animals the NA level was increased in the hypothalamus, the DA level in the striatum, and the 5-HT level in the hippocampus and striatum. Opposite changes were observed in the steady-state levels of the monoamines in the hippocampus and striatum as compared to those in the tolerant controls. The data suggest that the central monoamines may be involved in mediating the actions of neurohypophyseal peptides on ethanol tolerance.
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PMID:Brain monoamines are involved in mediating the action of neurohypophyseal peptide hormones on ethanol tolerance. 342 Nov 21


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