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

Vasopressin and oxytocin were measured by radioimmunoassay in rat posterior pituitary and microdissected hypothalamic areas after 3 and 10 days of oral 2 percent sodium chloride in place of drinking water. There was a significant decrease in concentration of both hormones in posterior pituitary and in specific areas of the hypothalamus. Supraoptic, paraventricular, and arcuate hypothalamic nuclei and the retrochiasmatic area had decreased concentration of one or both hormones following hypertonic saline, while hormone concentration in the suprachiasmatic nucleus and median eminence was unaffected.
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PMID:Vasopressin and oxytocin are depleted from rat hypothalamic nuclei after oral hypertonic saline. 93 63

Isolated rat neural lobes were incubated in vitro in Locke's solution containing anaesthetic quantities of urethane, pentobarbitone or tribromoethanol. The oxytocin content of the incubation medium was estimated before, during and after stimulation of the tissue by raising the potassium chloride concentration from 5-6 to 56 mmol/l. Urethane (25 mmol/l) significantly potentiated oxytocin release (P less than 0-01) whereas tribromoethanol (0-5 mmol/l) had no obvious effect and pentobarbitone (0-4 mmol/l) significantly (P less than 0-01) inhibited its release. Reduction of the sodium chloride concentration in the medium potentiated the release of oxytocin in each case but did not alter its pattern. Urethane which increased secretion of oxytocin also increased calcium ion uptake by the neural lobes and pentobarbitone which decreased oxytocin release decreased calcium ion uptake. The results may explain why the blood concentration of the neurohypophysial hormones tends to be higher in rats anaesthetized with urethane than with tribromoethanol. Inhibition of hormone release by pentobarbitone suggests that this anaesthetic is unsuitable for use in studies of neurohypophysial hormone release. A partial explanation of the anaesthetic properties of urethane and pentobarbitone may also have been found if the release of neurotransmitter substances is influenced in a similar manner.
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PMID:Potentiation by urethane and inhibition by pentobarbitone of oxytocin release in vitro. 110 67

The efflux of [3-H]GABA from glial cells in the rat posterior pituitary was followed in isolated glands incubated in the presence of 10-minus 5 M aminooxyacetic acid which is known to inhibit GABA metabolism. Electrical stimulation of the pituitary stalk evoked an increase in the rate of efflux of [3-H]GABA as did elevation of the extracellular potassium concentration. The release of neurophysin from nerve terminals in the gland was also increased by electrical stimulation. The increase in [3-H]GABA efflux appeared to be independent of frequency at 2, 5, or 25 HZ if the number of pulses delivered was kept constant, although stimulation at 10 HZ was more effective than either 2 or 25 HZ. The efflux of [3-H]GABA evoked by 56 mM K+ was inhibited by 50% when calcium was removed from the washing fluid and 3 mM EGTA added, while the response evoked by electrical stimulation was unaffected by this procedure. The electrically induced efflux of [3-H]GABA was inhibited by 50% when choline chloride was substituted for sodium chloride in the washing medium, although it was unaffected by tetrodotoxin (0.8 times 10-minus 6 g/ml). The release of exogenous GABA from the pituicyte glia is compared with that of neurophysin from the nerve terminals in the posterior pituitary, and the results are discussed with reference to possible mechanisms of the glial release process.
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PMID:The release of [3-H]gamma-aminobutyric acid and neurophysin from the isolated rat posterior pituitary. 113 91

Rats euhydrated and dehydrated for two or four days were given intracerebroventricularly (i.c.v.) thyrotropin-releasing hormone (TRH) in a daily dose of 200 ng dissolved in 10 microliters of 0.9% sodium chloride.) A single dose of TRH administered to euhydrated animals was followed by a significant increase of the vasopressin content in the neurohypophysis and hypothalamus as well as of the hypothalamic oxytocin content. On the contrary, a single dose of TRH decreased the oxytocin content in the neurohypophysis. Under conditions of dehydration TRH distinctly restrained the decrease of vasopressin and oxytocin in the hypothalamus. In animals dehydrated for two or four days the decrease of oxytocin in the neurohypophysis, brought about by stimulation of osmoreceptors, was distinctly more marked under treatment with TRH. On the contrary, the depletion of neurohypophysial vasopressin was significantly less apparent under such conditions. 28 nmol/L TRH markedly increased vasopressin release but inhibited that of oxytocin from the neurointermediate lobes incubated in vitro both under basal conditions as well as during stimulation with excess (56 mmol) potassium.
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PMID:Thyrotropin-releasing hormone (TRH) and vasopressin and oxytocin release: in vitro as well as in vivo studies. 130 67

In situ hybridization histochemistry and indirect immunofluorescence histochemistry were used to study changes in the expression of vasopressin (VP), oxytocin (OXY), tyrosine hydroxylase (TH), galanin (GAL), dynorphin (DYN) and cholecystokinin (CCK) in hypothalamic magnocellular neurons of the paraventricular (PVN) and supraoptic (SON) nuclei of rats. After prolonged administration of 2% sodium chloride as drinking water (salt-loading), the treatment increased the levels of VP, OXY, TH, GAL, DYN and CCK mRNA in the PVN and SON. The increase in CCK mRNA was, however, proportionally higher in the PVN than in the SON. Within cell bodies of the PVN and SON of salt-loaded rats, a depletion of VP- and OXY-like immunoreactivity (LI) and an increase in TH-LI were seen. In salt-loaded/colchicine-treated rats, a marked decrease in GAL- and DYN-LI, but no specific changes in CCK-LI were observed. Within nerve fibers of the posterior pituitary of salt-loaded rats, a marked depletion of VP-, GAL- and DYN-LI was found. Less pronounced depletion was observed in OXY- and CCK-LI, and no specific changes in TH-LI were seen. The results show that high plasma osmolality induces increased mRNA levels for VP, OXY, TH, GAL, DYN and CCK, presumably indicating increased synthesis, an increased export from cell somata of VP, OXY, GAL and DYN, and a decrease in levels of these peptides in the posterior pituitary, suggesting increased release. The catecholamine-synthesizing enzyme TH, however, which has a cytoplasmic localization and is not released from nerve endings, remains high in the cell bodies and nerve endings during this state of increased activity.
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PMID:Peptides and transmitter enzymes in hypothalamic magnocellular neurons after administration of hyperosmotic stimuli: comparison between messenger RNA and peptide/protein levels. 169 5

The effect of central osmotic stimulation on oxytocin (OT) secretion from the paraventricular nucleus (PVN) was examined using a newly developed in vivo microdialysis technique. A dialysis probe was inserted into the PVN region and microdialysis was performed in conscious animals. Hyperosmotic solutions were delivered via the dialysis probe, and perfusate and blood samples were collected. OT was consistently detected in the PVN dialysate. Hyperosmotic sodium chloride (1 M) produced a significant increase in dialysate and plasma OT, whereas D-mannitol (2 M) had no effect. These results suggest that (1) in vivo microdialysis may provide a useful technique for the evaluation of neuropeptide secretion from specific brain regions and (2) there are sodium-sensitive cells in the PVN region which respond to increases in extracellular sodium, resulting in an increase in central and peripheral oxytocin secretion.
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PMID:Extracellular oxytocin in the paraventricular nucleus: hyperosmotic stimulation by in vivo microdialysis. 210 21

1. Intracerebroventricular (I.C.V.) injections of isotonic and hypertonic solutions into the dorsal (D3V) and ventral (V3V) third ventricle were employed to examine the release of vasopressin (AVP) and the mean arterial pressure (MAP) response to elevated cerebrospinal fluid (CSF) osmolality in the conscious rat. 2. The D3V injection of hypertonic sodium chloride solution was associated with a concentration-dependent, transient increase in plasma AVP concentration and MAP. 3. The D3V injection of 5 microliters 0.85 M-sodium chloride elicited a 7-fold increase in plasma AVP and oxytocin concentrations, but had no effect on plasma ACTH concentration. The D3V injection of 1.11 M-mannitol in 0.15 M-sodium chloride had no effect on plasma AVP concentration or MAP. However, the D3V injection of 0.746 M-mannitol in 0.4 M-sodium chloride elicited a significant transient increase in plasma AVP, but had no effect on MAP. 4. The V3V injection of 5 microliters 0.85 M-sodium chloride elicited a prolonged increase in plasma AVP concentration and a transient increase in MAP. The V3V injection of 5 microliters 1.11 M-mannitol in 0.15 M-sodium chloride elicited an equal, but transient, increase in plasma AVP concentration, but had no effect on MAP. 5. The pressor effect of a D3V injection of 0.85 M-sodium chloride was unaffected by prior administration of the V1 (pressor) receptor antagonist (beta-mercapto-beta,beta-cyclopentamethylene propionyl1, O-Me-Tyr2, Arg8)-vasopressin. 6. These results indicate that osmotically induced AVP secretion may be mediated by both sodium receptors and osmoreceptors, although expression of the response may depend upon the maintenance of a 'permissive' concentration of sodium in the CSF. 7. It appears also that the pressor effect is not due to increased plasma AVP concentration, but only results from elevation of the CSF sodium concentration.
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PMID:The vasopressin response to centrally administered hypertonic solutions in the conscious rat. 212 Apr 29

In rats euhydrated or dehydrated for two or four days the neurohypophysial vasopressin and oxytocin content was estimated. Rats were given intracerebroventricularly (i.c.v.) isoprenaline in a daily dose of 10 micrograms dissolved in 10 microliters of 0.9% sodium chloride. The neurohypophysial vasopressor and oxytocic activity diminished progressively during deprivation of water. A single dose of isoprenaline diminished the neurohypophysial content of vasopressin in euhydrated rats. In animals dehydrated for two or four days the depletion of neurohypophysial vasopressin storage (as brought about by osmoreceptor stimulation) was distinctly less marked under treatment with isoprenaline. The neurohypophysial oxytocin storage was diminished by a single dose of isoprenaline; on the contrary, during dehydration isoprenaline distinctly intensified the oxytocin depletion in the neurohypophysis.
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PMID:The vasopressin and oxytocin content in the neurohypophysis under conditions of increased beta-adrenergic transmission in euhydrated and dehydrated rats. 217 1

1. The measurement of cellular mRNA content by quantitative in situ hybridization is a valuable approach to the study of gene expression in brain since this tissue exhibits a high degree of phenotypic heterogeneity. 2. The cellular content of vasopressin and oxytocin mRNA in hypothalamo-neurohypophysial system neurons was altered by maintaining rats for 24 hr on 2% sodium chloride water. 3. Statistical and graphical techniques were then used to analyze cell by cell how mRNA levels were altered as a result of osmotic stimulation. We propose that the negative binomial probability distribution is a suitable model to describe how mRNA content varies across a defined cell population. For both measures of oxytocin and vasopressin mRNA levels, maximum-likelihood estimation indicated that this model adequately described empirical findings obtained from rats drinking tap water or salt water. 4. Both graphical and statistical analyses suggested how the defined neural system responds to osmotic stimulation: mRNA content was altered as a multiplicative function of "initial state." The utility and limitations of the quantitative approach are discussed.
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PMID:Quantitative in situ hybridization to measure single-cell changes in vasopressin and oxytocin mRNA levels after osmotic stimulation. 233 46

Pulsatile administration of oxytocin was compared with continuous infusion of oxytocin for induction of labor in pregnant rats. The dosages consisted of intravenous injections of 0, 2.5, and 5 mU oxytocin every 10 minutes and intravenous infusion of 1 mU/minute of oxytocin in 0.9% sodium chloride. These doses are within the range of endogenously secreted pulses. All treatments began on day 22 at 2 p.m. and continued for 8 hours. Pulsatile administration resulted in a marked reduction in the dose of oxytocin required to induce labor. Using 5 mU pulses, birth was induced with 18.4%, and using 2.5 mU pulses, with 24% of the dose needed using continuous infusion. Parturition was advanced by 12 hours on the average by oxytocin treatment, but no significant differences were observed between the various oxytocin dosage regimens in this regard or in regard to gestation length, induction-delivery interval, duration of delivery, or the proportion of living or dead pups. Significantly more uterine activity was induced with each mU of oxytocin using pulsatile administration than using continuous infusion. There was no evidence for down-regulation of oxytocin receptors during a continuous infusion of oxytocin. We postulate that the greater efficacy of oxytocin pulses to induce uterine activity and delivery in comparison to continuous infusions is due to a more effective stimulation of prostaglandin F2 alpha release from the decidua. The amount of oxytocin needed for induction of labor with 2.5 mU pulses was similar to the decrease in neurohypophyseal oxytocin content during the first stage of spontaneous labor, and uterine activity elicited was also similar to that observed during spontaneous labor.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pulsatile administration enhances the effect and reduces the dose of oxytocin required for induction of labor. 271 12


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