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

Oxytocin administration in rat infused with hypotonic saline is associated with a saliuresis and altered renal water excretion. The role of vasopressin in determining the pattern of oxytocin-induced changes in urine flow was investigated in Long Evans and vasopressin-deficient Brattleboro rats, which exhibit contrasting diuretic and antidiuretic responses to oxytocin. Ethanol anaesthesia and water loading in Long Evans suppressed plasma vasopressin levels and was associated with an antidiuretic response to oxytocin. Vasopressin administration in the Brattleboro rat reversed the oxytocin-induced antidiuresis normally observed in vasopressin deficiency. These results taken with previous observations, have been interpreted as indicative that oxytocin acts as a weak agonist at the renal vasopressin receptor. When plasma vasopressin is suppressed or absent oxytocin acts as a weak antidiuretic agent, but in the presence of higher vasopressin levels a diuretic response to oxytocin is seen which follows displacement of vasopressin, the more potent antidiuretic agent, from the renal receptor.
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PMID:The influence of vasopressin on oxytocin-induced changes in urine flow in the male rat. 711 93

We have measured the concentrations of circulating oxytocin and the 13, 14-dihydro, 15-keto-metabolite of prostaglandin F2 alpha (PGFM) in women during preterm labor. Twelve women were given intravenous ethanol and 11 women received intravenous ritodrine for the prevention of preterm birth. Blood samples were obtained before and 1/2, 1, 2, 4, 12, and/or 24 hours after treatment began. On admission, the plasma concentrations of both oxytocin and PGFM were raised over levels observed in women with normal pregnancies of similar gestational age, 25 to 36 weeks. The initial oxytocin level was 58.5 +/- 8.2 pg/ml (mean +/- SE, n = 23) and the mean initial PGFM level was 264 +/ 33.1 pg/ml (n = 15); both values were significantly higher than in 10 control subjects (17.4 +/- 4.8 and 156 +/- 21.8 pg/ml, respectively). During infusion of ethanol, the plasma oxytocin level fell rapidly, the levels at 1/2 and 1 hour after infusion being significantly lower than before the infusion (29.0 +/- 5.5 and 27.8 +/- 3.5 pg/ml, respectively). The plasma oxytocin level remained low in women in whom the treatment arrested labor and prevented preterm birth (n = 8) but rose 2 to 4 hours after the infusion began in women in whom the treatment failed to arrest labor (n = 4). Ritodrine, on the other hand, had no significant effect on circulating oxytocin levels. The plasma PGFM level decreased significantly during ritodrine treatment only in the successfully treated patients. Ethanol had no consistent effect on plasma PGFM levels in the four patients in whom PGFM levels were measured. In the ritodrine-treated patients, the plasma PGFM level was positively correlated with the frequency of uterine contractions whereas in the ethanol-treated patients a correlation of plasma oxytocin to the frequency of contractions was observed. Thus, oxytocin secretion is increased during preterm labor, and the release of prostaglandin F is also increased. While it is not possible to determine whether any or both of these oxytocic agents actually trigger preterm labor, both seem to play a role in its mechanism.
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PMID:Plasma levels of oxytocin and 13, 14-dihydro-15-keto prostaglandin F2 alpha in preterm labor and the effect of ethanol and ritodrine. 714 97

Mice were rendered tolerant to the hypothermic effect of ethanol by forcing them to inhale ethanol vapor for 3 days. One day after withdrawal, tolerance was assessed by determining the response of the mice to an acute 3 g/kg IP challenge dose of ethanol. Thirty minutes before the injection of ethanol, saline or peptide solution was SC injected. The peptides studied were des-Gly9-Arg8-vasopressin (a peptide with reduced peripheral endocrine activities), oxytocin, and analogs and fragments of these peptides. None of the peptides, with the possible exception of oxytocin, affected body temperature in naive animals or the acute hypothermic response to ethanol in non-tolerant mice. Des-Gly9-Arg8-vasopressin enhanced the expression of tolerance to ethanol hypothermia; shorter fragments of vasopressin did not share this effect. Oxytocin attenuated the expression of tolerance but this may been due to an interaction with the acute effects of ethanol.
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PMID:Effects of peptides related to neurohypophyseal hormones on ethanol tolerance. 724 30

Intravenous ethanol infusion significantly reduced oxytocin-induced uterine activity in pregnant patients at term. The dose response to oxytocin was linear when plotted log2 x in all patients studied, and the line was shifted to the right by alcohol, but the slope remained essentially unchanged. These results suggest that alcohol directly inhibits the effect of oxytocin on the myometrium, although the possibility of some central inhibition of oxytocin release cannot be discounted.
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PMID:The inhibitory effect of ethanol on oxytocin-induced labor at term. 733 73

The effects of cholinoceptor agonists and neurotoxins on the release of vasopressin and oxytocin have been investigated in water-loaded rats under ethanol anaesthesia. Release of vasopressin was monitored by antidiuretic responses accompanied by increased urinary excretion of vasopressin. The rate of excretion of oxytocin-like radioimmunoreactivity was measured as an indicator of oxytocin release. Both nicotine and cytisine caused a preferential release of vasopressin. The release by nicotine was not inhibited by alpha- or neuronal-bungarotoxin. Neosurugatoxin blocked the release by cytisine. Comparison with the effects of these agents on combinations of alpha and beta subunits expressed in oocytes suggests that the central cholinoceptors mediating release of vasopressin are similar to those at autonomic ganglia and may contain a beta 4 subunit.
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PMID:The effect of cholinoceptor agonists and neurotoxins on the release of vasopressin in the rat in relation to the subunit composition of the cholinoceptor. 779 61

The effects of acute ethanol administration on the ingestion of NaCl and food were assessed in adult rats subjected to 1-hr drinking and feeding tests 30 min after intraperitoneal administration of ethanol. Ethanol pretreatment did not induce spontaneous NaCl ingestion, but significantly potentiated angiotensin II-stimulated salt appetite, but not water intake, in a dose-dependent manner. Similarly, ethanol pretreatment significantly potentiated neuropeptide Y-stimulated food intake in nonfasted rats, but did not, by itself, cause spontaneous food ingestion. Ethanol pretreatment also significantly blunted pituitary secretion of oxytocin in response to multiple excitatory stimuli. Finally, administration of oxytocin intracerebroventricularly prevented the ethanol-induced potentiation of salt appetite elicited by angiotensin II. In view of our previous findings that central oxytocin secretion inhibits both NaCl and food intake, we propose that ethanol potentiates the ingestion of various solutes in rats, in part, by inhibiting brain-projecting oxytocinergic pathways concurrently with its well-known effects to inhibit pituitary oxytocin secretion.
Alcohol Clin Exp Res 1994 Aug
PMID:Acute effects of ethanol on ingestive behavior in rats. 797 5

Ethanol ingestion affects the hypothalamo-neurohypophysial system resulting in increased diuresis, dehydration and hyperosmolality. We studied the supraoptic nucleus, of the hypothalamus, in ethanol-treated rats, to determine if ethanol alone and/or the associated disturbances of water metabolism lead to structural alterations in a nucleus known to play a central role in fluid homeostasis. Groups of male and female rats were ethanol-treated until 12 and 18 months of age and compared with age-matched pair-fed controls. Twelve and 18-month-old control groups and 12-month-old water control groups (rats submitted to chronic dehydration) were also included in this study in an attempt to differentiate between the effects of undernutrition and dehydration/hyperosmolality, and the specific neurotoxic effects of ethanol. We estimated the volume of the supraoptic nucleus and the numerical density of its neurons and calculated the total number of supraoptic neurons. The volume of both supraoptic neurons and neuropil were also estimated. In immunostained material the ratio of vasopressin to oxytocin neurons and the cross-sectional areas of the two neuronal types were evaluated. There was marked neuronal loss in alcohol-treated rats, but the volume of the supraoptic nucleus was increased. The increase in the volume of the supraoptic nucleus correlated with and was due to increases in the volume was particularly marked for vasopressin neurons. No significant differences were found between controls and pair-fed controls in any of the parameters investigated. In water control rats, the volume of the supraoptic nucleus and of the supraoptic neurons and neuropil was also greater than in pair-fed controls. However, the variations found were not as marked as in ethanol-treated rats and there was no cell loss. These findings reveal, for the first time, that chronic ethanol consumption affects the morphology of supraoptic neurons and neuropil and, consequently, the structure of the entire supraoptic nucleus. Moreover, this study supports the view that ethanol has direct neurotoxic effects on supraoptic neurons because the alterations that occur are not mimicked in animals in which water metabolism alone is disturbed.
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PMID:Effects of chronic alcohol consumption and of dehydration on the supraoptic nucleus of adult male and female rats. 825 26

The effect of haemorrhage and melatonin on the vasopressin and oxytocin storage in the neurohypophysis of pinealectomized male rats was determined. Sham operated or pinealectomized rats as well as rats pinealectomized and injected with melatonin (100 micrograms/100 g b. w., once daily over 8 days) or with melatonin vehicle (2.2% ethanol in 0.9% NaCl) were subsequently subjected to haemorrhage. Pinealectomy was followed by known decrease of both vasopressin and oxytocin content in the neurohypophysis as compared to sham operated rats. Similarly, haemorrhage decreased the neurohypophysial vasopressin and oxytocin storage in both sham operated and pinealectomized animals. Melatonin, injected to pinealectomized animals, did not modify the diminution of neurohypophysial vasopressin and oxytocin content caused by bleeding. The results demonstrate that in pinealectomized rats melatonin does not affect the rate of the response of vasopressinergic and oxytocinergic neurones to bleeding.
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PMID:The effect of haemorrhage and melatonin on neurohypophysial vasopressin and oxytocin content in pinealectomized male rats. 836 10

The progesterone antagonist mifepristone (RU 486) was injected i.m. into ewes during the early luteal phase of the oestrous cycle to test the hypothesis that duration of uterine exposure to progesterone from the corpus luteum initiates luteolysis through the proper timing of endometrial oxytocin receptor expression and pulsatile secretion of PGF2 alpha coincident with release of luteal oxytocin. In Expt 1, duration of cycle, the PGF2 alpha metabolite 15-keto-13,14-dihydro-PGF2 alpha (PGFM) and oxytocin concentrations were measured in ewes treated on days 5, 6, 7 and 8 of the oestrous cycle with either 2.5 or 5.0 mg RU 486 kg-1 day-1 (n = 4 per group); control ewes (n = 6) were injected i.m. with 80% ethanol (diluent). In Expt 2, the presence of functional uterine oxytocin receptors was determined indirectly on day 12 of the cycle by measuring the plasma PGFM response to oxytocin challenge (20 iu, i.v.) in diluent-treated ewes (n = 3) and in ewes treated with 2.5 mg RU 486 kg-1 day-1 on days 6, 7 and 8 of the oestrous cycle. Duration of the oestrous cycle of control ewes (16 +/- 1 days) was extended beyond day 24 (day 0 = oestrus) in 10 of 11 ewes treated with RU 486 as determined by daily exposure of ewes to a ram and by measurement of progesterone concentrations in plasma in the two experiments.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Failure of luteolysis and extension of the interoestrous interval in sheep treated with the progesterone antagonist mifepristone (RU 486). 841 Aug 10

We investigated the activity of phospholipase D (PLD) in human amnion cells labeled with [3H]oleate. The PLD activity was detected as signal-induced synthesis of phosphatidic acid (PA) and in the presence of ethanol, phosphatidylethanol (PEt). The PLD was shown to be activated by phorbol, 12-myristate, 13-acetate (PMA), calcium ionophore A23187, oxytocin, bombesin and bradykinin, but not by platelet-activating factor (PAF) and epidermal growth factor (EGF). The amniotic PLD thus appeared to be activated by a variety of agonists but with a certain specificity to stimulators. We examined the mode of the PLD activation using PMA (20 nM) and bradykinin (1 microM) as model stimulators. PMA and bradykinin elicited a rapid and sustained response with the peaks of PA-labeling attained at 5 and < 1 min after stimulation, respectively. In both cases, there was a concomitant rise of diacylglycerol (DG), and the PA accumulation was suppressed by ethanol at the expense of labeling of PEt. The PA synthesis caused by the two stimulators was similarly inhibited by staurosporine and by a chronic treatment with PMA (100 nM for 24 h), suggesting that the activation of PLD is linked to the action of protein kinase C. With the cells labeled with radioactive choline and ethanolamine, we found that the amniotic PLD hydrolyzed almost equally phosphatidylcholine and phosphatidylethanolamine. Although bradykinin and PMA stimulated cellular PLD to a comparable extent, prostaglandin (PG)E2 release was not stimulated by bradykinin in contrast to the marked effect by PMA. Further work is thus needed to clarify the significance of the novel PLD signaling pathway in the function of amnion cells.
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PMID:Phospholipase D activity of human amnion cells stimulated with phorbol ester and bradykinin. 850 57


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