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

Corpora lutea from cyclic ewes were dissociated by collagenase and trypsin/EGTA treatments, and enriched fractions of small and large luteal cells were prepared on gradients of Ficoll. These fractions were incubated separately or remixed before incubation. Colchicine, cytochalasin B and the calcium channel-blocker verapamil significantly reduced progesterone production by both small and large luteal cell fractions, while isoprenaline stimulated an increase in progesterone production by large luteal cell fractions only. When fractions of small and large luteal cells were remixed, no more and no less progesterone was produced than would have been predicted from equivalent fractions incubated separately. There was therefore no evidence of synergism between small and large luteal cells in the production of progesterone. Prostaglandin F-2 alpha, which can inhibit LH-stimulated progesterone production by ovine luteal tissue in vitro, had no effect on LH-stimulated progesterone production by small luteal cell fractions, but significantly inhibited that by enriched fractions of large luteal cells. Since large luteal cell fractions were contaminated with small luteal cells, which are probably responsible for the progesterone-secretory response of these fractions to LH, it was concluded that the inhibition of LH-stimulated progesterone production by small luteal cells is dependent on the presence of large luteal cells. Oxytocin added to large and small luteal cell fractions did not affect progesterone production by either fraction. It was therefore concluded that the inhibitory action of PGF-2 alpha on LH-stimulated progesterone production may require the interaction of large and small luteal cells, but that oxytocin is not likely to be an intermediary in this interaction.
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PMID:Do small and large luteal cells of the sheep interact in the production of progesterone? 386 69

Cervical specimens were obtained by needle biopsy in connection with caesarean section at term pregnancy. The preparations were superfused in an organ chamber and contractions were registered isometrically. Prostaglandin (PG) E2 and F2 alpha inhibited spontaneous contractions. The stimulatory action of noradrenaline was not influenced by PGF2 alpha but was reduced by PGE2 whereas both PGs abolished the excitatory effect of oxytocin.
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PMID:Effects of PGE2 and PGF2 alpha on the simulation by noradrenaline and oxytocin of human cervical muscle activity at term. 386 43

1 In the rat isolated uterus maximal spontaneous contractions and maximal sensitivity to angiotensin II, oxytocin and prostaglandin F(2alpha) were observed in di- and proestrus. Minimal sensitivity to the three agonists was observed in metoestrus. Maximal contractile effects of angiotensin II, oxytocin and prostaglandin F(2alpha) were thus observed when the ratio oestrogen/progesterone levels was high.2 The oestrogen-dependent sensitivity of the rat uterus is partially mediated by endogenous prostaglandins. Indomethacin suppressed the increased sensitivity to angiotensin and oxytocin present in dioestrus and proestrus but did not affect that to prostaglandin F(2alpha). Polyphloretin phosphate at a concentration of 10 mug/ml resulted in complete identity of dioestrus and metoestrus dose-response curves to angiotensin and oxytocin.3 Spontaneous uterine contractions observed when oestrogen levels are high are also dependent on intramural prostaglandins as they were inhibited by indomethacin and polyphloretin phosphate. In the metoestrus uterus, prostaglandin F(2alpha) induced the reappearance of spontaneous contractions.4 Prostaglandin F(2alpha) had a potentiating effect on angiotensin-elicited contractions which persisted after washing out prostaglandin F(2alpha).
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PMID:Effects of prostaglandin inhibitors on angiotensin, oxytocin and prostaglandin F2 alpha contractile effects on the rat uterus during the oestrous cycle. 437 38

The interaction of the ovarian steroid hormones (estrogen and progesterone) and the polypeptide hormone of posterior pituitary origin (oxytocin) appear to regulate the ovine estrous cycle by controlling production of the uterine luteolytic hormone PGF2 alpha. From our results, it appears that these steroid hormones may control PGF2 alpha release by regulating the availability of receptors for oxytocin in the endometrium, the primary site of PGF2 alpha production. Secondarily the ovarian steroid hormones may also regulate basal endogenous levels of oxytocin in the blood stream which may reinforce the luteolytic release of PGF2 alpha. Similar mechanisms may also be operative during the initiation of parturition in which steroid hormones, OT, and PGF2 alpha appear to play major roles (26). In addition to the known interdependence of steroid hormones and the gonadotropins (FSH, LH, and prolactin) required to initiate follicular growth, ovulation, and CL function, there appears to be a second interdependence required to terminate the ovarian cycle via the uterine luteolytic hormone PGF2 alpha, namely by the interaction between ovarian steroids and the posterior pituitary hormone, OT. Thus for both the initiation and termination of the ovarian cycle, there is evidence of a close interaction between the ovary and brain.
Adv Prostaglandin Thromboxane Res 1980
PMID:Hormone receptor control of prostaglandin F2 alpha secretion by the ovine uterus. 624 81

Prostaglandin (PG) E2 was the major PG released from the superfused guinea-pig uterus on Day 7, followed by in descending order 6-oxo-PGF1 alpha, thromboxane (TX) B2 and PGF2 alpha. However, the outputs of all four substances were low and were very similar. By Day 15, PGF2 alpha output from the superfused uterus had increased 21.9-fold, whereas the outputs of PGE2, 6-oxo-PGF1 alpha and TXB2 had increased only 1.8-, 2.9- and 1.2-fold, respectively. A mechanism is apparently "switched on" between Days 7 and 15 which causes a fairly specific increase in the release of PGF2 alpha from the uterus. Progesterone and/or estradiol had no effect on PG or TX release when superfused over the uterus on Day 7, nor did they have any effect on PG and TX release from the Day 15 uterus when administered separately. When administered together, however, they significantly inhibited PGF2 alpha, PGE2 and 6-oxo-PGF1 alpha, but not TXB2, release from the Day 15 uterus. Oxytocin had no effect on PG release from the Day 7 or Day 15 uterus, while A23187 stimulated PGF2 alpha, 6-oxo-PGF1 alpha and, to a lesser extent, PGE2 release from the uterus on both Days 7 and 15. Oxytocin is apparently not important for stimulating PGF2 alpha release from the guinea-pig uterus in relation to luteolysis, whereas increasing intracellular free Ca++ levels may be part of the mechanism for "switching on" uterine PG synthesis. Furthermore, changes in intracellular free Ca++ levels in the endometrium may be responsible for the pulsatile nature of PGF2 alpha release from the uterus.
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PMID:Prostaglandin release from the guinea-pig uterus superfused in vitro. Effect of stage of estrous cycle, progesterone, estradiol, oxytocin and A23187. 640 12

It is possible to induce labour in pathological pregnancies after artificial ripening of the cervix. The present study concerns 70 patients (45 primipara, 25 multipara). The main pathologies are hypertension of pregnancy and pregnancies past dates. Prostaglandin F2 alpha has been used with a Tylose gel containing 5 mg of PGF2 alpha introduced by the extra-amniotic route. The cervical change was noted using Bishop's score. The mean increase of the cervical score was 0.8 with the first PGF2 alpha gel. The total mean increase was 1.2. Two cases of hyperstimulation of the uterus were observed and they led to Caesarean section. Prostaglandin gel induced labour in 56% of the patients. The mean time between the introduction of the gel and the delivery was 14 h for primipara and 10 h for multipara. Other patients were induced with oxytocin on the following day. Epidural analgesia was widely used in this study (in 64% of cases). The mean duration of labour was 6 h 10 for primipara and 4 h 30 for multipara. 30% of the patients needed Caesarean section but there was a marked difference between primipara (36%) and multipara (4%). After a review of the literature the authors conclude that it is useful to ripen the cervix prostaglandin but, as foreign authors do, they think that PGE2 should be more efficient.
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PMID:[Maturation of the cervix uteri using prostaglandin F2 alpha before induction of labor in pathologic pregnancies]. 657 95

In a prospective randomized study, 36 patients with spontaneous rupture of the membranes of greater than or equal to 4 h duration were stimulated with 3 mg vaginal prostaglandin E2 pessaries or intravenous oxytocin. Oxytocin stimulation was associated with shorter labours and a lower incidence of abnormal cervimetric progress. Of the patients given prostaglandin pessaries, 40% required a second dose after 4 h for slow progress; 45% of the primigravidae subsequently developed abnormal labour which was corrected by augmentation with oxytocin in all cases. One caesarean section was carried out for disproportion, and the remaining 35 patients were delivered vaginally. Prostaglandin pessaries were not associated with an increased incidence of hyperstimulation or sepsis. In conclusion, although PGE2 pessaries are safe in spontaneous rupture of the membranes, intravenous oxytocin is more efficient in stimulating labour.
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PMID:Controlled study comparing vaginal prostaglandin E2 pessaries with intravenous oxytocin for the stimulation of labour after spontaneous rupture of the membranes. 657 7

Prostaglandin (PG) F2-alpha was administered extraamnially to 70, and intraammially to 51 pregnant women to induce abortion in the 14th to 28th weeks of pregnancy. With intraamnial infusion of PGF2-alpha (25 mg/8-12 hours), the mean induction time was 27.1 hours and thus, oxytocin, too, was required in 19.6% of the cases. With extraamnial infusion of 5 mg PGF2-alpha at 4 to 6 hour intervals, mean induction time was 34.0 hours and addition of oxytocin was required in 46.1% of the cases. Moreover, if 15 to 30 mg of PGF2-alpha was infused at 18 to 29 hour intervals, or 1 mg at 2 hour intervals, the induction of abortion was considerably prolonged. In primigravidae, or in the 14th to 18th weeks pregnancy, the abortive effect of PGF2-alpha was weaker than in multigravidae or in the 19th to 28th weeks of pregnancy. In the case of intrauterine fetal deaths, the abortive effects was more marked than in intact pregnancies. After extraamnial infusion of PGF2-alpha, the uterine contractions were less coordinated than after intraamnial dosage. In about one-third of abortion induced by extraamnial PGF2-alpha, the fetal heart was found to work for 5 to 15 minutes after abortion.
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PMID:Abortion-inducing effect of prostaglandin F2-alpha in the mid-trimester of pregnancy. 659 19

Prostaglandin (PG)F2 alpha, in the dose range 1-10(4) nM, failed to elicit oxytocin secretion in vitro from ovine luteal tissue on day 12 of the estrous cycle (estrus = Day 0), during a 60 minute period. Preincubation of luteal slices for 6 hours prior to treatment suggested that tissue desensitization due to the release of endogenous prostaglandins by tissue preparation is not responsible for this lack of response. However, in luteal tissue collected on day 6 of the ovine estrous cycle, PGF2 alpha stimulated oxytocin release in a dose-dependent manner. This apparent change in sensitivity of the ovine corpus luteum in vitro may be due to a combination of a reduction in the luteal oxytocin available for release and saturation of PGF2 alpha receptors in the more mature tissue.
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PMID:Prostaglandin F2 alpha-induced release of oxytocin from ovine corpora lutea in vitro. 787 93

High concentrations of PGF2 alpha and PGE2 are produced by the uterus during the early postpartum period in cows and may play an important role in both placental separation and uterine involution. In the present study, we have examined the hormonal and intracellular control mechanisms involved in PGF2 alpha and PGE2 secretion by caruncular and allantochorionic tissue in vitro. Tissue explants, obtained about 6 hr postpartum from cows that delivered normally (NFM, n = 10) or cows with retained fetal membranes (RFM, n = 4), were incubated for 6 hr and PGF2 alpha and PGE2 concentrations in the medium were determined by radioimmunoassay. Addition of oxytocin (100 microU/ml), platelet activating factor (PAF, 100 ng/ml) and epidermal growth factor (EGF, 100 ng/ml) had no effect on secretion of PGF2 alpha from the caruncle, but oxytocin and PAF did stimulate PGE2. There was no difference between groups of cows. All three substances stimulated PGF2 alpha from the allantochorion of NFM, but not RFM, cows and stimulated PGE2 secretion from the allantochorion of both groups of cows. Incubation of the tissues with cholera toxin (100 ng/ml), dibutyryl cyclic adenosine 3',5'-monophosphate (dibutyryl cAMP, 1 mM), calcium ionophore A23187 (5 microM) or phorbol ester 12-myristate-13 acetate (PMA, 100 nM) showed that PGF2 alpha secretion is essentially via the calcium-protein kinase C effector pathway. However, calcium-protein kinase C and cAMP second messenger systems appear to be involved in the secretion of PGE2. Prostaglandin secretion was sensitive to cycloheximide in both caruncular and allantochorionic tissues, suggesting that protein synthesis may be involved. In conclusion, these data show that in vitro PGF2 alpha secretion can be modulated by the agonists used only in allantochorion and is essentially via the calcium-protein kinase C effector pathway. PGE2 secretion can be modified in both caruncular and allantochorion tissues and involves both inositol triphosphate-diacylglycerol and cAMP second messenger systems.
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PMID:Control of in vitro prostaglandin F2 alpha and E2 synthesis by caruncular and allantochorionic tissues from cows that calved normally and those with retained fetal membranes. 804 99


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