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

1 In the anaesthetized lactating rat, the suckling of the young causes the regular release (about every 7 min) of brief pulses of oxytocin (0.5 to 1.0 mu), which each produce a single transient increase in intramammary pressure.2 The effects of several cholinoceptor antagonists were studied in relation to this natural reflex, and also the release of oxytocin evoked by the intraventricular injection of cholinomimetics.3 Reflex milk ejection was blocked by the nicotinic antagonists mecamylamine and hexamethonium, and the inhibition was dose-dependent (ED(50) of 1 mg/kg i.v. and 5 mg/kg i.v., respectively). Despite the use of high doses, the muscarinic antagonists atropine (200 mg/kg), hyoscine (90 mg/kg) and benzhexol (30 mg/kg) all failed to prevent the reflex release of oxytocin.4 Acetylcholine (20 to 100 mug), bethanechol (0.2 to 4.0 mug) and carbachol (0.01 to 0.2 mug) injected into the cerebral ventricals stimulated a sustained release of oxytocin, which produced multiple increases in intramammary pressure. Nicotine (200 mug) was relatively ineffective by this route.5 The release of oxytocin by intraventricular bethanechol or carbachol was abolished by atropine (0.1 to 1.0 mg/kg) but not by mecamylamine (5 mg/kg) or hexamethonium (5 mg/kg).6 None of the antagonists used significantly affected either the release of oxytocin following electrical stimulation of the neurohypophysis or the mammary sensitivity to endogenous or exogenous oxytocin.7 The results suggest that the neural pathway controlling the reflex release of oxytocin during suckling in the rat contains a cholinergic component, which acts through nicotinic receptors. A second cholinergic pathway, of the muscarinic type, may also exist. The role of these two pathways is discussed.
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PMID:Effects of cholinoceptor antagonists on the suckling-induced and experimentally evoked release of oxytocin. 56 1

Nicotine stimulation, induced by cigarette smoking, has previously been identified as a potent stimulus for vasopressin release in humans. In this study, radioimmunoassay measurements of plasma vasopressin and human neurophysin were performed on samples taken from 14 normal subjects during cigarette smoking. Significant rises in vasopressin occurred in 10 of the 14 subjects and the same 10 had significant rises in neurophysin. Pretreatment with ethanol in 3 subjects either eliminated or greatly blunted the responses of both vasopressin and neurophysin to cigarette smoking. These studies indicate that the release mechanisms for vasopressin and neurophysin are closely linked in humans.
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PMID:Nicotine-stimulated release of neurophysin and vasopressin in humans. 120 97

Bovine granulosa cells were cultured in a defined serum-free system to examine their responsiveness to acetylcholine (ACh). Continuous exposure to concentrations of ACh between 10(-8)-10(-4) M resulted in dose-dependent increases (up to 6.7-fold) in the secretion of oxytocin and progesterone, with an ED50 of 6.6 microM. Ascorbic acid (0.5 mM), a known stimulator of granulosa secretion, synergized with ACh, resulting in an increase in the amounts of hormone secreted and a 7-fold increase in cellular sensitivity to ACh (ED50 = approximately 0.9 microM). Treatment of cells with ACh for 24 h at various times during a typical 5-day culture resulted in a stimulation that persisted for up to 4 days after removal of ACh. Carbachol (10(-8)-10(-4) M), a receptor antagonist with both antimuscarinic and antinicotinic actions, had no distinct effect on hormone secretion by the cells, but the effects of 10(-5) M ACh could be completely abolished by equimolar or hypomolar concentrations of the specific muscarinic receptor antagonists atropine and scopolamine. Nicotine bitratrate (10(-8)-10(4) M), a dose-dependent nicotinic receptor agonist/antagonist, had no effect on the cells. It is concluded that bovine granulosa cells, exhibiting a luteinized phenotype in culture, are responsive to cholinergic agonists in a specific and saturable manner. The response of the cells is probably mediated through muscarinic receptors and has both medium and long term (persistent) components. These results indicate that cholinergic neurotransmitters may play a direct role in the regulation of ovarian function in the ruminant.
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PMID:Cholinergic stimulation, through muscarinic receptors, of oxytocin and progesterone secretion from bovine granulosa cells undergoing spontaneous luteinization in serum-free culture. 229 62

1. Strips of longitudinal muscle can be obtained from guinea-pig ileum either retaining or free from Auerbach's plexus.2. The denervated strip is unresponsive to electrical stimulation by brief shocks, whether given singly or in trains; it also fails to respond to nicotine or dimethylphenylpiperazinium iodide (DMPP), and eserine causes no spasm.3. Denervated strips neither contain detectable acetylcholine (< 0.4 ng/mg), nor release it spontaneously (< 5 pg/mg/min) or in response to stimulation (< 31 pg/mg/min). The acetylcholine metabolism of the innervated strip is therefore that of the adherent Auerbach's plexus. Innervated strips had a mean acetylcholine content of 28 ng/mg, a mean resting output of 94 pg/mg/min and an output in response to stimulation at 10 c/s of 700-1200 pg/mg/min.4. By comparing the responses of innervated and denervated strips it was concluded that arecoline, methylfurmethide, alpha,beta-ethylal-gamma-tri-methylammonium propanediol iodide (2268 F), muscarine, histamine, tremorine, oxytocin, and substance P, like acetylcholine, act primarily on the smooth muscle directly; and that angiotensin, barium, potassium, m-bromophenyl choline ether and 5-hydroxytryptamine have a progressively increasing proportionate effect on the nerve plexus. Nicotine and DMPP were inactive in the absence of the plexus.5. The longitudinal muscle with its accompanying plexus contains about one quarter of the acetylcholine of the whole ileum, and is responsible for about one fifth of the output to electrical stimulation.6. The volley output of acetylcholine by the innervated strip declines sharply as rate of stimulation increases. Output of acetylcholine was reduced by morphine and by cocaine, particularly when resting or when stimulated at low rates.7. Acetylcholine output by whole ileum from guinea-pig declines in the absence of glucose, but is insulin-independent. Output by strips of ileum from rats made diabetic with alloxan was similar to that from normal rats.8. The similarity in properties of acetylcholine output from innervated strips, where it must come from nervous tissue, to that from whole ileum, and the insulin-independence of output from whole ileum suggest that the whole of the acetylcholine output of intestine is nervous in origin.9. Comparison of the acetylcholine metabolism of the innervated strip with that of the superior cervical ganglion suggests that the typical features of the former (high resting output, high volley output at low rates, low minute output at high rates of stimulation, and sensitivity to morphine) may be linked with the absence of specialized neuro-effector junctions and represent a relatively primitive transmission process.
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PMID:The origin of acetylcholine released from guinea-pig intestine and longitudinal muscle strips. 429 53

The effect of nicotine on the ultrastructural changes and hormone contents of the neural lobe of the pituitary were studied in the rat. Nicotine caused a significant release of both vasopressin and oxytocin from the neural lobe. The examination of the neural lobe with electron microscope reveals the nerve terminals depleted of neurosecretory granules. These results suggest that a definite correlation exists between hormone contents and ultrastructural morphology.
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PMID:Ultrastructural changes in the neural lobe of the rat pituitary following nicotine pretreatment. 668 53

For the study on initiation of labor, a highly sensitive and specific radioimmunoassay for oxytocin (OT) was developed. Investigations were performed on the blood levels of OT and neurophysins in women during labor, lactation as well as in umbilical vessels. The blood was assayed for OT and Estrogen Stimulated Neurophysin (ESN), Nicotine Stimulated Neurophysin (NSN) in each specific radioimmunoassay. The mean value of plasma OT levels of women without labor pains (5 minutes interval) ws 217.3 +/- 36.02 (pg/ml, Mean +/- S.E.) whereas the values at 28 to 40 weeks of gestation was much lower than those. At delivery the OT level in maternal plasma was 176.3 30.92 and 207.5 62.90 in the umbilical vein respectively. There was no statistical difference in the level of OT before and after lactation. ESN level was higher during lactation and NSN level showed the similar pattern. At delivery NSN concentration in the umbilical artery was higher than that in the vein. These data suggest that hypothalamo-pituitary function correlate with labor and lactation.
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PMID:[Study on blood levels of oxytocin and neurophysins during labor and lactation (author's transl)]. 724 67

An adolescent boy with essential hypernatremia, absent corpus callosum, mental retardation, hypodipsia, and partial diabetes insipidus with "inappropriate" ADH regulation and secretion was studied regarding factors controlling ADH and neurophysin release. Persistent hyperosmolality was noted while on 100 mEq sodium intake daily. Endogenous vasopressin activity was demonstrated after prolonged water deprivation. Hypertonic saline infusion produced increased volumes but dilute urine. Aqueous pitressin increased urinary osmolality, decreased serum osmolality, urine flow rate, and free water clearance. Stable water diuresis was induced by water loading and on normal saline infusion. Nicotine-stimulated neurophysin remained unexpectedly low and below the level of detectability when sampled during the physiologic studies, whereas oestrogen-stimulated neurophysin was elevated during oestrogen stimulation, water loading, and orthostasis procedures. Plasma vasopressin was suppressed with water loading but remained suppressed 90 min after tilt table testing. These data indicate impairment of the osmoreceptor mechanism: however, since the patient had a normal response of oestrogen-stimulated neurophysin, that part of the neurohypophysis appears intact. Chlorpropamide was effective in alleviating the hyperosmolar state acutely and maintained normal osmolar concentrations during two years of therapy.
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PMID:Essential hypernatraemia, antidiuretic hormone and neurophysin secretion: response to chlorpropamide. 746

The rapid secretion of ACTH in response to nicotine is mediated by a central mechanism involving brainstem catecholaminergic regions. To identify specific brainstem regions involved in activating the hypothalamo-pituitary-adrenal axis and other areas of the brain by iv nicotine, immunocytochemical detection of cFos protein was used as a marker for neuronal activation. Nicotine (0.05 mg/kg) stimulated cFos expression in the parvocellular paraventricular nucleus (pcPVN; containing CRH-positive neurons mediating ACTH secretion); this correlated with the expression of cFos in the A2 (norepinephrinergic) and C2 (epinephrinergic) regions of the brainstem nucleus tractus solitarius, which project directly to the pcPVN. The selectivity of this brainstem activation was shown by the absence of responses in the locus coeruleus (LC), A1, and C1 catecholaminergic regions to this low dose of nicotine. In contrast, a high dose of nicotine (0.1 mg/kg), which produced a brief episode of tremor, was required for expression of cFos in the LC. This was associated with a further increase in the number of cFos-positive cells in the PVN, primarily through recruitment in the magnocellular region, a known projection field of LC. The higher dose of nicotine also induced cFos in the vasopressinergic region of the supraoptic nucleus (SON), whereas the lower dose of nicotine exclusively induced cFos in the oxytocinergic region of the SON. Limbic regions that receive catecholaminergic inputs, such as the the central nucleus of the amygdala (involved in PVN regulation) and the cingulate gyrus of the cortex, showed a dose-dependent increase in the number of cFos-positive cells after nicotine, whereas the dentate gyrus of the hippocampus only responded to the high dose. Thus, nicotine is a potent and selective stimulus for neuronal activation in brainstem catecholaminergic regions and their projection fields in the pcPVN and SON, which regulate the hypothalamo-pituitary-adrenal axis and vasopressin/oxytocin secretion, respectively.
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PMID:Nicotine stimulates the expression of cFos protein in the parvocellular paraventricular nucleus and brainstem catecholaminergic regions. 838 11

The actions of nicotine, hexamethonium, and ethanol on the hypothalamo-hypophysial system have been investigated in the rat. The antidiuretic action of nicotine was not inhibited by ethanol, nor by doses of hexamethonium which were sufficient to block both its pressor and convulsant actions. Hexamethonium itself had an antidiuretic action the mechanism of which has been investigated. Nicotine caused a release of oxytocin into the blood which was not blocked by ethanol nor significantly reduced by hexamethonium. The results suggest that any synapse which exists at the supraoptic nuclei is dissimilar in its pharmacological properties to synapses at autonomic ganglia.
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PMID:The effects of nicotine, hexamethonium and ethanol on the secretion of the antidiuretic and oxytocic hormones of the rat. 1348 75