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

Isolated uteri from rats with regular 4-day cycles were incubated in Krebs-Ringer bicarbonate buffer and the release of PGF into the medium was measured by radioimmunoassay after extraction of the incubation medium with ethyl acetate at pH 3.0-3.5. PGF was produced from endogenous precursors and accumulated in equal amounts in the medium during two successive 60 min periods on each day of cycle, but the magnitude of the production varied significantly during the cycle, being greatest in estrus. Oxytocin in doses up to 500 mU/ml had no effect on PGF accumulation in the incubation period at any stage of the cycle, while epinephrine (10(-3)) greatly stimulated PGF release from the estrous uterus but had no effect on PGF release from the diestrous uterus. Phentolamine, an alpha-blocking agent, had no effect on the epinephrine-induced release of PGF, while propranolol, a beta-blocking agent, not only prevented in increase in PGF production induced by epinephrine but also reduced the basal release of PGF by the estrous uterus. Since oxytocin contracts and epinephrine relaxes the nonpregnant rat uterus both in vivo and in vitro, it is unlikely that the effects of these two compounds on uterine contractility are mediated by the release of PGF2alpha.
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PMID:Effects of epinephrine and oxytocin on the release of prostaglandin F from the rat uterus in vitro. 56 31

The author studied the uterine reactivity of alloxan-diabetic rats to oxytocin. Using the Magnus method with Ringer-Locke nutrient solution (modified by Garcia de Jalon) low in calcium and varying the bath temperature from 30 degrees C to 36 degrees C, modifications of the organ were observed. The dose-effect relationship was only practicable in uterus of normal rats at 30 degrees C. When the bath temperature reached 35 degrees C, it was only possible to evaluate the uterine reactivity of alloxan rats by fixed periods of rhythmical contractions, that were graphically represented. This modification in the experiment resulted from the absence of reactivity of the alloxanic rat organ at 30 degrees C. Besides describing the methodology applied, the author suggests a hypothesis about the role of Ca++ on the variation of uterine reactivity. A previous administration of diethylstilbestrol (estrogenic hormone) in alloxanic rats, not treated with insulin, was followed by recovery of uterine reactivity, reinforcing the hypothesis of the mobilization of Ca++ in discompensated alloxan-diabetic rats as a factor of variations on the sensibility of the tissues.
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PMID:[Uterine reactivity of alloxan-diabetic rats to oxytocin (author's transl)]. 56 68

The effect of enflurane on uterine contractility was studied in sexually mature rabbits in which intrauterine balloon catheters had been implanted. Three animal groups were studied: untreated; treated with estrogen-progesterone; and 27 to 28 days pregnant. The effects of 1.5 percent or 3.0 percent enflurane were quantitated by measuring contraction frequency and amplitude during an anesthetically steady state. The effects of prior anesthesia with 1.5 percent enflurane on uterine responses to 1.5 IU oxytocin IV were also evaluated. Neither 1.5 percent of 3.0 percent enflurane altered contraction amplitude or frequency in the 3 groups of rabbits. However, the amplitude of the contractile response to oxytocin 30 minutes following enfluane was significantly depressed. The results indicate that, while the intact rabbit uterus under different hormonal influences is not depressed by 1.5 or 3.0 percent enflurane, its response to oxytocin following enflurane is decreased.
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PMID:Enflurane and uterine contractility in rabbits. 56 51

Responsiveness of the rat uterus on the day of estrus to PGE2, PGF2alpha and oxytocin was increased by administration of PGF2alpha i.p. 24 hours prior to the experiments, but that of the uterus on the day of diestrus was not altered by the same treatment. The delayed action of PGF2alpha was not observed in the uterus of ovariectomized rats, but was observed in the uterus of estrogen treated rats. The delayed action of PGF2alpha was not evident in either the vas deferens or the intestine of the rat.
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PMID:[Influence of estrogen on the delayed action of prostaglandin F2alpha on the rat uterine contraction (author's transl)]. 56 95

1. A technique is described for obtaining a myometrial preparation devoid of endometrium, from the uterus of the rat in oestrus. 2. Acetylcholine and prostaglandin F2alpha (PGF2alpha) produced concentration-effect curves with the same maximal tensions and slope on the whole uterus and myometrial preparations. Concentration-effect curves to bradykinin and oxytocin on the myometrial preparation were altered, resulting in a shift to the right and a decreased maximum response compared with those produced by the whole uterus. 3. Indomethacin produced greater antagonism of the responses of the whole uterus to bradykinin and oxytocin than to acetylcholine and PGF2alpha, whereas responses of the myometrium to all four agonists were similarly depressed. 4. Responses of the myometrial preparation to a range of concentrations of bradykinin and oxytocin were significantly enhanced by prior sensitization of the myometrium to PGF2alpha. This significant enhancing effect of PGF2alpha was only seen with the threshold dose of acetylcholine. 5. It appears that the mechanism of action of bradykinin and oxytocin on the rat uterus involves both a direct action and an indirect action. The indirect action possibly involves release of prostaglandin(s) from the endometrium.
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PMID:The action of bradykinin and oxytocin on the isolated whole uterus and myometrium of the rat in oestrus. 56 12

Electromyograms were obtained from three different locations on the uterus of conscious, unrestrained rats during the 4 day estrous cycle. Intrauterine pressure changes were monitored simultaneously by means of indwelling intraluminal balloons (vol. 0.02 to 0.05 ml.). Electrical activity consisted of bursts of action potentials that were usually initiated at either end of the uterus. Propagated burst activity gave rise to cyclic intrauterine pressure changes, whereas bursts appearing at one electrode only did not elicit any measurable contractions. The rate of intrauterine pressure development depended on the propagation velocity, whereas the tension achieved was related to the duration of burst activity. All three parameters of electrical activity studied, namely, the duration and frequency of spike bursts, as well as their rate of propagation, varied significantly during the cycle. Regional differences were also subject to cyclic variations; thus, in proestrus the bursts originated predominantly at the cervical end, whereas in diestrus they were usually initiated at the ovarian end. Oxytocin stimulated the frequency and duration of bursts along the whole uterus and elicited corresponding changes in intrauterine pressure. Response to oxytocin was dose dependent and modified by cycle stage. Norepinephrine caused a transient prolongation of burst activity that was not dose dependent; epinephrine had a marked dose-dependent inhibitory action. The response to catecholamines did not vary significantly during the cycle. The variations in electrical and mechanical activity were characteristic for each stage of the ovarian cycle and could be correlated with the well-known hormonal changes. High circulating estrogen levels in proestrus are associated with infrequent but rapidly propagated spike bursts, whereas low levels in estrus are associated with frequent and sometimes nonpropaged bursts. The rise in plasma estrogen in diestrus coincides with a decrease in the frequency of burst activity, and the elevated progesterone levels are probably causally related to the significant drop in propagation velocity and the increase in duration of bursts observed in diestrus. These findings are consistent with the concept that estrogen withdrawal activates the estrogen-primed, quiescent myometrium, and that progesterone has an effect similar to that of estrogen withdrawal--at least in the rat.
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PMID:Electrical and mechanical activity of rat uterus in vivo during the estrous cycle. 56 83

The effect of some mammary gland diseases, of the act of sucking and of machine milking on spontaneous uterine activity was studied in cows during their early puerperal period by use of the radiotelemetric method. It was established that clinical catarrhal and suppurating mastitis block spontaneous uterine activity. However, the uterus preserves its reactivity to oxytocin which is confirmed by injection of the hormone. The act of sucking and machine milking have a positive effect on spontaneous uterine activity up to the 5--7 days following calving. Uterine contractions are registered after reflectory influences too. The number and amplitude of uterine contractions 48 h after calving are closely correlated with the predisposition of uterine musculature to post calving complications.
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PMID:[Effect of mammary gland diseases, the act of sucking and machine milking on utering motility in cows during the early puerperal period. I]. 57 44

Paired segments of rat uterus were treated in vitro with relaxin (W1164-3, 150 GPU/mg) until the amplitude of contraction was reduced to at least 50% of the pre-treatment amplitude. Test segments then received 100 ng of either PGE1, PGE2, PGF2alpha or 250 uU of oxytocin. Control segments remained untreated. There was a significant increase in contraction amplitude in response to the spasmogens (P less than 0.05) but no increase was seen in controls.
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PMID:In vitro response of relaxin-treated rat uterus to prostaglandins and oxytocin. 59 78

Intrauterine pressure was monitored in vivo in oestrogen-treated ovariectomized ewes before, during and after treatment with progesterone (50 mg s.c./day for 3 days). Progesterone reversibly reduced the frequency and amplitude of myometrial activity and abolished uterine reactivity to oxytocin (i.v.) and PGF-2alpha (intrauterine infusion). The rate of rise of intrauterine pressure during active pressure cycles was significantly reduced. These results confirm that the action of progesterone on the ovine myometrium is comparable to the classic progesterone 'block'. The intrauterine infusion of PGF-2alpha (10 microgram/min), which elicited a marked mechanical response in the control animals, failed to stimulate the progesterone-'blocked' uterus, suggesting that the inhibition produced by progesterone is due to a direct action of the hormone on the uterine muscle and not to an indirect mechanism operating through endometrial prostaglandin output.
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PMID:Demonstration that progesterone 'blocks' uterine activity in the ewe in vivo by a direct action on the myometrium. 62 2

[1-Deaminopenicillamine,4-threonine]oxytocin was prepared in duplicate from S-benzyl-3-mercapto-3,3-dimethylpropanoyl-Tyr(Bzl)-Ile-Thr(Bzl)-Asn-Cys(Bzl)-Pro-Leu-Gly-NH2 (I) by removal of the Bzl-protecting groups with Na-NH3, followed by cyclization of the resulting disulfhydryl compound with K3Fo(CN)6. The analogue was purified by desalting on Sephadex G-15 in 50% acetic acid and gel filtration of Sephadex G-15. The protected peptide I was synthesized (a) by the solid-phase method and (b) by a combination of solid-phase synthesis and an [8 + 1] coupling in solution. The analogue has no detectable agonist activity in rat vasopressor or isolated rat uterus assays. It has an antivasopressor pA2 of 6.67 +/- 0.09. It is a potent inhibitor of the in vitro oxytocic response to oxytocin and has a pA2 value of 7.46 +/- 0.04. (Material from the repeat synthesis has a pA2 value of 7.59 +/- 0.08.) Thus the substitution of threonine for glutamine in the antagonist [1-deaminopenicilliamine]oxytocin (pA2, 7.14 +/- 0.05) has effected a twofold increase in inhibitory potency. [1-deaminopenicillamine,4-threonine]oxytocin is one of the most potent inhibitors of oxytocin known to date.
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PMID:[1-Deaminopenicillamine,4-threonine]oxytocin, a potent inhibitor of oxytocin. 62 12


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