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

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

Urethan-anesthetized rats were used to identify effective stimuli for the release of the peptides arginine vasopressin (AVP) and oxytocin into the ventral septal area (VSA) of the brain. Febrile responses to intracerebroventricular injection of prostaglandin E1 (PGE1) were observed in rats whose body temperatures were maintained at 35, 37, or 39 degrees C. Microinjection of the AVP antagonist d(CH2)5Tyr(Me)AVP into the VSA enhanced fever only when PGE1 administration was associated with a significant rise in body temperature. Passive elevation ("artificial fever") or reduction of body temperature in the absence of a PGE1 stimulus was not affected by the antagonist. Push-pull perfusion of the VSA and the dorsal hippocampus, followed by radioimmunoassay of perfusates for AVP and oxytocin, revealed enhanced release into the VSA of AVP only when PGE1 administration was followed by a rise in body temperature. Oxytocin was released whenever body temperature was raised. Peptide concentrations in simultaneous perfusates of dorsal hippocampus did not change in response to PGE1 administration or to passive elevation of body temperature. We conclude that AVP is released into the VSA, but not the dorsal hippocampus, of the rat during a fever induced by PGE1. Oxytocin is released into the VSA, but not the hippocampus, when temperature is elevated.
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PMID:Vasopressin and oxytocin in rat brain in response to prostaglandin fever. 224 Feb 66

Urethane anaesthetized male rats were given an i.p. injection of hypertonic saline to increase plasma osmotic pressure. This injection resulted in significantly elevated plasma oxytocin levels and increased discharge activity of putative oxytocin cells in the supraoptic nucleus. Subsequent injection of naloxone (1 mg/kg) i.v. resulted in a similarly large increase in plasma oxytocin, but did not affect the discharge activity of putative oxytocin neurones. The results suggest that, following an i.p. injection of hypertonic saline, endogenous opioids act at the neurosecretory terminals to partially inhibit oxytocin release.
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PMID:Effects of naloxone and of intraperitoneal hypertonic saline upon oxytocin release and upon supraoptic neuronal activity. 339 34

The potency of opiates for suppressing oxytocin release relative to their potency as analgesics was tested in lactating rats. Oxytocin release was evoked by the sucking of the young in urethane-anaesthetized and unanaesthetized rats, and was detected by the characteristic behaviour of the young and milk yield respectively. The tail-flick test, using noxious radiant heat, was used to assess analgesia. Intraperitoneal injection of morphine (1 mg kg-1 and 5 mg kg-1) significantly reduced milk yield in unanaesthetized rats. Urethane-anaesthetized rats displayed a pattern of reflex milk-ejection responses similar to that found in conscious rats. This reflex was significantly inhibited in a dose-related, naloxone-reversible manner by buprenorphine (ED50 0.18 mg kg-1), meptazinol (ED50: 14.0 mg kg-1), morphine (ED50: 0.67 mg kg-1), pentazocine (ED50: 15.0 mg kg-1) and pethidine (ED50: 7.9 mg kg-1). Although intraperitoneal injection of morphine (5 mg kg-1) abolished the increase in intramammary pressure occurring at reflex milk-ejection, that evoked by intravenous oxytocin (0.5-1 mu) was unaffected. Each opiate also caused significant, dose-related, naloxone-reversible increases in tail-flick latency. The ED50 doses were buprenorphine (ED50: 0.14 mg kg-1), meptazinol (ED50: 12.5 mg kg-1), morphine (ED50: 5.0 mg kg-1), pentazocine (ED50: 12.5 mg kg-1) and pethidine (ED50: 6.1 mg kg-1). The order of potency for analgesia and for suppression of oxytocin release were identical, namely: buprenorphine greater than morphine greater than pethidine greater than meptazinol greater than pentazocine. The results obtained with lactating rats suggest that secretion of the hormone oxytocin is substantially reduced during opiate-induced analgesia.
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PMID:A comparison of analgesia and suppression of oxytocin release by opiates. 654 45

Two experiments were performed to study the effects of bromocriptine and alpha-ergocryptine on oxytocin secretion in lactating rats. In both experiments, after overnight separation from their litters, rats were injected with either vehicle alone or ergot alkaloid plus vehicle; 4 h later the litters were returned. In the first experiment the mothers were conscious. Treatment did not affect suckling behaviour, number of stretch reactions or little weight gain in the first 30 min. Oxytocin injection before the second 30 min period of suckling caused no extra milk to be obtained. In the second experiment the mothers were anaesthetized with ethyl carbamate (1.1 g/kg body weight) at the time of the ergot alkaloid or vehicle injection. Changes in intramammary pressure were recorded during suckling. Ergot alkaloids altered neither the number of milk ejections caused by suckling, nor the proportion of milk ejections equivalent to 0.2 millimicron or more oxytocin. In both experiments treatment with ergot alkaloids suppressed secretion of prolactin. It is concluded that (a) in suppressing lactation, bromocriptine and alpha-ergocryptine do not inhibit oxytocin secretion as well as prolactin secretion, and that (b) prolactin secretion is not a necessary concomitant of oxytocin secretion.
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PMID:Bromocriptine and alpha-ergocryptine do not inhibit oxytocin secretion in the lactating rat. 689 7

Recent studies have shown that the neuropeptides arginine-8-vasopressin (AVP) and oxytocin (OXT) are released within the supraoptic (SON) and paraventricular (PVN) nuclei of the hypothalamus in response to microdialysis of these nuclei with high-NaCl perfusion media. These results suggest an inherent osmosensitivity of SON and PVN neurons. To investigate whether the observed release of AVP/OXT is a unique phenomenon to these neuropeptides, several brain regions were examined for the release of amino acids or dopamine in response to high- or low-NaCl stimulation. Urethane-anesthetized male Sprague-Dawley rats were perfused with five-ion solution using U-shaped microdialysis probes. Samples were collected at 30-min intervals and analyzed for amino acids and dopamine by HPLC. In the dialysates of all perfusion areas, including the SON, PVN, hippocampus, and striatum, concentrations of Asp, Glu, Ser, Gln, Gly, taurine (Tau), and gamma-aminobutyric acid (GABA) were significantly increased during perfusion with high-NaCl medium. This release was found to be dose dependent when tested in the hippocampus and striatum with perfusion medium containing 0.5 or 1.0 M NaCl. However, only the release of Glu and Ser was found to be Ca2+ dependent. In contrast, the use of mannitol, a nonionic osmolyte, for perfusions in the striatum in concentrations of 0.5 and 1 M resulted in reduced levels of amino acids in the dialysates (Glu, Ser, Gln, and Tau). Low-NaCl perfusion medium (0.01 M) resulted in significantly increased Glu, Tau, Gly, and GABA levels in the striatum. In addition, dopamine levels in striatal dialysates were significantly increased during stimulation with 1 M NaCl. These results indicate that stimulation with high NaCl concentrations affects the release of several neurotransmitters and is not specific for AVP and OXT. The described phenomenon of the release of amino acids in response to this stimulation seems to be a response to the changed ionic concentration rather than to the osmolality. In light of these findings shown for amino acids and dopamine as well as those previously reported for AVP, OXT, and angiotensin, it would appear that sensitivity to tonicity changes brought about by microdialysis may be a feature of many transmitter systems.
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PMID:Microdialysis with high NaCl causes central release of amino acids and dopamine. 789 Oct 91

Interleukin-1 beta stimulates oxytocin and vasopressin release in conscious, male rats and causes a rise in blood pressure. These experiments were done to : A) examine the effect of i.c.v. interleukin-1 beta (1 ng/microliter) on circulating levels of vasopressin in female rats at different stages of lactation and B) determine if alpha-adrenergic mechanisms and/or prostaglandins were involved as mediators. Urethane-anaesthetized nonlactating rats and rats at Day 7, 10, 20 and 26 of lactation were set up for arterial blood sampling and i.c.v. injections. One mL blood samples were obtained in one min periods before, and at 1, 2.5, 5, 10, 30, 60 and 120 min after the following treatments: i.c.v. treatment with either interleukin-1 beta (1 ng in 1 microliter PBS-BSA) or PBS-BSA (1 microliter) as a vehicle control; or i.c.v. treatment with interleukin-1 beta following pretreatment with either phentolamine (1.7 micrograms/microliter i.c.v.) or indomethacin (1 microgram/microliter i.c.v.). As blood was sampled, isotonic saline was infused (1 mL per min) and blood pressure was monitored to minimize any hypovolemic effects due to sampling. Extracted plasma was assayed using a specific vasopressin radioimmunoassay. Interleukin-1 beta i.c.v. stimulated the release of vasopressin above that elicited by PBS-BSA alone in non-lactating rats resulting in an approximate 1.2 to 2-fold increase in plasma hormone levels. Throughout the first half of lactation, vasopressin responsiveness to i.c.v. interleukin-1 beta treatment was markedly attenuated. In latter stages of lactation, the response recovered and resembled that of non-lactators around the time of weaning. Prostaglandins consistently mediate a stimulatory action of interleukin-1 beta on vasopressin release whereas alpha-adrenergic mechanisms mediate a depression of interleukin-1 beta-induced vasopressin release during the early to middle stages of lactation. It is possible that the depression in interleukin-1 beta-stimulation of vasopressin release in early to mid-lactation is conducive for nursing to occur and that the increase in vasopressin responsiveness towards the latter stages of lactation represents a component of the weaning process.
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PMID:Changing effect of i.c.v. IL-1 beta on vasopressin release in anaesthetized, female rats at different stages of lactation: role of prostaglandins and noradrenaline. 895 69