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)

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

The effects of graded doses of a substituted tripeptide analogue of the C-terminal part of oxytocin, D-Pip-Leu-GlyNH2 (DPLG), were investigated on the development of tolerance to the hypothermic effect of and dependence on alcohol in mice. Ethanol injection (4 g/kg i.p.) repeated on 3 consecutive days led to the development of tolerance in control and peptide-treated (0.005 microgram/mouse) animals. In the latter group, however, the level of tolerance was lower than in the control animals. The higher doses (0.05-5.0 micrograms/mouse) inhibited the development of tolerance. Repeated peptide administrations (5, 25, 125 micrograms/animal) did not affect the development of the dependence on alcohol which resulted from combined daily injections of tert-butanol (1.5 g/kg i.p.) and ethanol (3 g/kg i.p.). The severity of withdrawal was quantified via the convulsions induced with different doses of picrotoxin. When the peptide was injected only before the testing of withdrawal, DPLG markedly prolonged the onset of withdrawal signs.
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PMID:D-pipecolyl-leucyl-glycinamide, a substituted tripeptide analogue of the C-terminal part of oxytocin, influences tolerance to and dependence on ethanol in mice. 377 81

A clinical test was conducted with 40 healthy women 2-8 days following parturition to assess the effect of ethanol on the milk-ejecting reflex. The women before they were given alcohol were used as their own controls. The inhibition was found to be better correlated with the dose of ethanol administered than with the blood alcohol concentration measurement conducted at the end of the experiment. Results are tabulated and graphed. Ethanol in doses from .5-.93 gm per kilogram produced significant inhibition of the milk-ejecting activity; in doses from 1-1.48, there was an inhibition of the response to suckling; in doses from 1.5-1.9, the strongest inhibition was observed. The study, thus, confirms earlier findings that ethanol blocks oxytocin release. The effect was widely variable but definitely dose-related. It is possible that doses higher than 2 gm per kilogram could completely inhibit the suckling-induced oxytocin release which controls milk-ejecting activity.
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PMID:Effect of different doses of ethanol on the milk-ejecting reflex in lactating women. 468 84

It is well documented that children with the fetal alcohol syndrome are a direct consequence of heavy maternal ethanol consumption during pregnancy. The mechanism by which ethanol exerts its teratogenic effect is however, far from understood. Recent experimental evidence has shown alcohol to have a direct inhibitory effect on embryogenesis. Little information, however, is available concerning other factors associated with maternal drinking which may contribute to abnormal fetal development. Proper materno-fetal hormonal balance is essential to insure successful pregnancy outcome. Of particular importance with respect to normal fetal development, are the levels of placental tropic hormones; pituitary hormones such as prolactin and oxytocin; adrenal cortical hormones; both maternal and fetal thyroid hormones; maternal and fetal sex hormones; and maternal insulin. Ethanol alters the levels of a variety of hormones associated with the hypothalamic/pituitary-gonadal, -adrenal and -thyroid axes. Many of these alterations have been observed in the male, however, with little data available on the female. In spite of the known adverse effect of ethanol on certain aspects of female reproductive function, few if any studies have examined the effects of alcohol ingestion during pregnancy on maternal endocrine balance. It is hoped that the present review will provide a rationale for the examination of alcohol effects on maternal endocrine hormones, as well as to provide possible target areas with respect to fetal development subsequent to ethanol-induced endocrine imbalance.
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PMID:Endocrine balance as a factor in the etiology of the fetal alcohol syndrome. 701 43

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

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.
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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

Large conductance, Ca(2+)-activated K+ channels are believed to underlie interburst intervals and, thus, contribute to the control of hormone release from neurohypophysial terminals. Because ethanol inhibits the release of vasopressin and oxytocin, we studied its effects on large conductance, Ca(2+)-activated K+ channels from these terminals using patch-clamp techniques. Ethanol (10-100 mM) applied to the cytosolic surface of excised, inside-out patches reversibly increases channel activity in a concentration-dependent manner, reaching a plateau at 50-100 mM. This activation is not mediated by freely diffusible cytosolic second messengers or the release of Ca2+ from intracellular stores. Rather, it likely reflects a direct interaction of ethanol with the channel protein or a closely associated component. Neither the unitary conductance nor the characteristics of the voltage-current relationship are modified by the drug. The increase of channel activity by ethanol results from a modification of channel gating properties: the contribution of long openings to the total time spent in the open state is increased, the average duration of the fast openings is slightly increased, and long closures disappear in the presence of the drug. The activation of large conductance, Ca(2+)-activated K+ channels by ethanol, in conjunction with the previously reported inhibition of voltage-dependent Ca2+ channels, can explain the reduced release of vasopressin and oxytocin after ethanol ingestion.
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PMID:Ethanol increases the activity of large conductance, Ca(2+)-activated K+ channels in isolated neurohypophysial terminals. 856 10

Abstract We tested the hypothesis of a cross-inhibition of oxytocin (OT) release by endogenous opioid peptides co-released with vasopressin (VP). This opioid cross-inhibition resulted in a selective block of OT release and hence in preferential release of VP. The effects of the opiate receptor antagonist naloxone were tested on neurohypophyseal VP release during dehydration, ethanol administration and sulphated cholecystokinin octapeptide (CCK-8S) application, assuming that the inhibition of pituitary OT release by endogenous opioids increases as neurohypophyseal VP output increases. A high VP output was found to coincide with increased inhibition of OT release: Subcutaneous injection of graded doses of naloxone (30 min prior to decapitation), augmented OT plasma levels significantly more in 24 h water-deprived male rats than in normally hydrated rats. Naloxone had no effect on VP release. Ethanol (10% in saline) administered intragastrically 50 min prior to decapitation and 20 min before subcutaneous naloxone (5 mg/kg) resulted in the inhibition of VP output. The ethanol treatment resulted in a rise in plasma OT levels that was additional to the effect of naloxone. These features were present in normally hydrated as well as in 24 h water-deprived animals, but were more pronounced in the latter group. Peripheral CCK-8S administration induces an abrupt and selective secretion of OT. Blocking the opioid inhibition of OT release with naloxone resulted in a significant rise of OT compared to that with CCK-8S alone. The magnitude of the opioid inhibition coincided with the activity of the VP system, and a higher dose of naloxone was needed to potentiate the CCK-8S effect on OT release in the water-deprived group than in euhydrated rats. No effect of CCK-8S and/or naloxone was found on VP plasma levels. The data indicate that opioid peptides co-released with VP (like dynorphin) may be responsible for cross-inhibition of OT release during dehydration. This suggests that dynorphin acts in a paracrine way, making it a strong candidate for this role.
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PMID:Enhanced Neurohypophyseal Vasopressin Release is Associated with Increased Opioid Inhibition of Oxytocin Release. 1921 47


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