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 possible inhibition exerted by ethanol on the oxytocin response to breast stimulation was tested in normal women. The possible role of endogenous opioids in the control of the oxytocin response to breast stimulation and/or ethanol action was also examined. Sixteen normal women were tested four times on the 22nd day of four consecutive regular menstrual cycles. All women underwent mechanical breast stimulation (for 10 min) with the concomitant administration of normal saline, naloxone (2 or 4 mg in an iv bolus plus 5 or 10 mg over 16 min), ethanol (50 ml in 110 ml of whisky po) or the combination of ethanol and naloxone. Plasma oxytocin levels rose about twofold after breast stimulation, with a mean peak response at 10 min. The oxytocin response to breast stimulation was not changed by the treatment with the lower (2 plus 5 mg) or the higher (4 plus 10 mg) dose of naloxone, whereas it was completely abolished by ethanol. However, when ethanol was given together with naloxone, the oxytocin rise induced by breast stimulation was only partially inhibited by ethanol (the mean oxytocin peak was 50% higher than baseline). At both doses naloxone produced similar effects. These data demonstrate that ethanol inhibits the oxytocin response to breast stimulation. Naloxone sensitive endogenous opioids do not appear to be involved in the control of the oxytocin rise induced by breast stimulation. In contrast, since naloxone partially reversed the inhibiting effects of ethanol, a partial involvement of opioid peptides in ethanol action is supposed.
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PMID:Inhibition by ethanol of the oxytocin response to breast stimulation in normal women and the role of endogenous opioids. 157 49

Inhibition of ethanol tolerance by oxytocin has been demonstrated previously using the hypothermic effect only. The purpose of the present experiment was to investigate the effect of oxytocin on the development of tolerance to ethanol-induced hypothermia, myorelaxation and akinesia in mice. Four groups of mice received daily intraperitoneal injections of saline or oxytocin (0.005 mg) plus saline or ethanol (2 g/kg). The peptide was administered 2 hours before ethanol. For five consecutive days, temperature measurements were performed 20 minutes before and after ethanol injection. Myorelaxation and akinesia were evaluated following the second temperature measure. Oxytocin pretreatment, which had no intrinsic effects, resulted in a robust selective attenuation of tolerance to ethanol-induced hypothermia, myorelaxation and akinesia. These results suggest that the mechanisms for peptide modulation are common to these three typical effects of ethanol.
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PMID:Oxytocin attenuates tolerance not only to the hypothermic but also to the myorelaxant and akinesic effects of ethanol in mice. 180 28

The effects of EtOH on peptide release and on high-threshold, voltage-activated calcium (Ca++) channels were examined in acutely dissociated rat neurohypophysial terminals. These terminals release the peptide hormones, arginine vasopressin (AVP) and oxytocin. Release of AVP from isolated intact neurohypophyses, induced by either electrical stimulation or elevated potassium, was inhibited by clinically relevant concentrations of EtOH. "Whole-cell" patch-clamp recording methods were used to study the effects of EtOH on voltage-activated Ca++ currents (ICa) in the peptidergic nerve terminals. Amplitudes of both fast-inactivating ICa and long-lasting ICa were reduced in EtOH, and the reduction in ICa did not result from a shift in its current-voltage or steady-state inactivation relationships. Only the fast-inactivating component recovered after removal of EtOH. The effects of EtOH on ICa could not be attributed to changes in osmolarity. In contrast to ICa, the fast, transient K+ current was insensitive to EtOH. These results suggest that EtOH-induced reduction of ICa in the peptidergic nerve terminals produces a decrease in AVP release, resulting in lowered plasma AVP levels.
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PMID:Calcium currents and peptide release from neurohypophysial terminals are inhibited by ethanol. 194 19

In rats, a syndrome of yawning and penile erection results from the administration of low doses of apomorphine, a dopamine receptor agonist shown to stimulate dopamine autoreceptors. Ethanol has been shown to influence dopamine metabolism. Low doses of ethyl alcohol (0.25 mg./kg.) failed significantly to alter apomorphine-induced yawning or penile erection, while 0.5 mg./kg. decreased erectile behavior but did not significantly alter the number of yawns. A reduction in both yawning and penile erection in response to apomorphine challenge was seen after the acute intraperitoneal injection of relatively high doses (1.0-3.0 mg./kg.) of ethanol. Two possible mechanisms of action may explain these phenomena. Alcohol may interfere with dopaminergic receptor mechanisms, or conversely, alcohol, through its actions on central dopamine metabolism may alter a second neurotransmitter/neuropeptide more directly responsible for the production of apomorphine-induced yawning and penile erection, possibly oxytocin.
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PMID:The impact of alcohol ingestion on erections in rats as measured by a novel bio-assay. 198 89

Arginine vasopressin is a neuropeptide that has been shown to modulate functional ethanol tolerance and memory processes. These actions of vasopressin in the CNS have been shown by us and others to be mediated by V1 receptors. Intracerebroventricular injection of vasopressin in mice resulted in a substantial increase in mRNA for the proto-oncogene c-fos in septum and hippocampus, but no increase in cerebral cortex. A V1-selective agonist also increased septal c-fos mRNA levels, while a V2-selective agonist was less effective. Similarly, the response to vasopressin was more effectively blocked by a V1- than a V2-selective antagonist. These results indicate that vasopressin acts specifically at V1 receptors in mouse septum and hippocampus to increase c-fos mRNA. The vasopressin metabolite, AVP(4-9), also increased c-fos mRNA levels in septum and hippocampus, while the response to oxytocin, which has different effects from vasopressin on memory and tolerance, was greater in hippocampus than in septum. Nerve growth factor, in contrast to the other peptides, had a more pronounced effect on c-fos mRNA levels in cerebral cortex than in the other brain areas. Increased c-fos expression has been hypothesized to play a role in neuroadaptation, and these results suggest that modulation of septal c-fos expression could be important for vasopressin effects on ethanol tolerance and/or memory.
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PMID:Arginine vasopressin induces the expression of c-fos in the mouse septum and hippocampus. 216 40

The maturity of the hypothalamic-neurohypophyseal system in the first 10 days of the postnatal life of rats was analysed through the potential inhibitory effect of ethanol on oxytocin and vasopressin secretion. Experimental animals were intraperitoneally injected with ethanol, and the control ones with the corresponding amount of physiological solution. Hypophyses were extracted 30 min later to be histologically analysed. Although the morphological features of neurohypophysis with functionally active pituicytes and dense vascular net were present even from the first natal day, neurosecretory grains were noticed not before the 8 th day. But the inhibitory effect of ethanol on neurosecretion did not manifest itself until the 10 th day, so it can be concluded that in this period the hypothalamic-neurohypophyseal system had not yet reached its level of complete maturity. Fatty acids in pituicytes being elements of neurohypophyseal neuroglia are pronunced even in animals younger than 10 days, which indicates that their origin could not be necessarily linked to the process of neurosecretion. In acutely alcoholized offsprings the amount of fatty acids in the neurohypophysis was reduced. This is substantiated by the engagement of the alcohol dehydrogenase (ADH) and the microsomal ethanol-oxidizing system (MEOS) in alcohol metabolism with which follows retarded oxidation process of fatty acids.
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PMID:[Reactive characteristics of the neurohypophysis in the early postnatal period]. 228 3

1. In water-loaded rats under ethanol anaesthesia, the injection of 2-4 microliters 1.54M NaCl solution (hypertonic saline:HS) into a lateral cerebral ventricle (i.c.v.) produced an antidiuretic and a pressor response, together with increased urinary excretion of vasopressin and 'oxytocin-like radioimmunoreactivity' (OLRI). In lactating rats HS also produced a milk-ejection response which was shown to be due to the release of oxytocin. 2. The injection of 20-40 micrograms gamma-aminobutyric acid (GABA) or 40-80 ng muscimol i.c.v. 2 min before HS inhibited the antidiuretic, pressor and milk-ejection responses and reduced the urinary excretion of vasopressin and OLRI. 3. The pressor response to HS was abolished by a ganglion blocking agent but it was not reduced by a vasopressin antagonist. After the antagonist, the antidiuretic response to HS was abolished and the pressor response was accompanied by a diuresis both of which were blocked by muscimol. 4. The threshold dose of HS for an antidiuretic response was 4-8 times higher on injection into the cisterna magna (i.cist.) than when injected i.c.v. GABA, i.v. or i.cist, did not inhibit the response to HS i.c.v. 5. The results confirm other evidence that, in the rat, in contrast some other species, an osmotic stimulus causes release of both vasopressin and oxytocin. This release is blocked by GABA and muscimol. These drugs and HS act at a site reached not from the subarachnoid space but from the cerebral ventricles, probably the hypothalamus. The pressor response to HS under the experimental conditions used is due entirely to central sympathetic stimulation and this effect, as well as the release of vasopressin and oxytocin, is blocked by muscimol.
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PMID:Central inhibition by gamma-aminobutyric acid and muscimol of the release of vasopressin and oxytocin by an osmotic stimulus in the rat. 233 82

Chromatographic behaviour of oxytocin has been studied. A simple and convenient technique has been developed for preparative purification of oxytocin using silica and ethanol. The product obtained contains not more than 3% impurities and has activity about 450 IU/mg.
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PMID:[High performance liquid chromatography of peptide bioregulators, their fragments and derivatives. IV. Chromatographic behavior and purification of oxytocin]. 259 Feb 51

The effects of intracerebroventricularly (icv.) administered oxytocin (OXT) and lysine-8-vasopressin (LVP) on the development of hypothermic tolerance to ethanol were investigated. Mice equipped with an icv cannula were pretreated with graded doses of OXT or LVP (3 ng, 300 pg, 30 pg or 3 pg/animal) before the daily intraperitoneal ethanol (4 g/kg) injection. Two doses of OXT or LVP (3 ng or 300 pg/animal) blocked the development of hypothermic tolerance to ethanol. Smaller doses of the peptides were ineffective in inhibiting the gradual decrease in hypothermia upon repeated ethanol administration, which effect was observed in the control group. The data presented show that the central administration of these neurohypophyseal peptides blocks the development of tolerance to ethanol.
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PMID:Intraventricular administration of neurohypophyseal hormones interferes with the development of tolerance to ethanol. 271 43


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