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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Oxytocin infusions were initiated on day 10 of the oestrous cycle in ewes, and luteal regression was induced by injection of 100 micrograms cloprostenol on day 12. Blood samples were collected at frequent intervals via an indwelling jugular vein cannula to measure concentrations of progesterone and luteinizing hormone (LH) during the luteal and follicular phases in saline (n = 6) and oxytocin (n = 5) infused animals. The oxytocin infusion maintained peripheral plasma concentrations of 53 +/- 3.2 pg oxytocin ml-1 (mean +/- SEM) compared with values of about 1 pg ml-1 during oestrus in control ewes. Oxytocin infusion had no effect on luteal phase progesterone concentrations, the timing of luteolysis, basal luteinizing hormone (LH) secretion, LH pulse frequency, or the timing or height of the LH surge. Treated ewes came into oestrus significantly earlier than controls (P < 0.05) but ovulated normally. Uterine samples collected 96 h after cloprostenol injection (approximately day 2 of the cycle) showed that oxytocin receptor concentrations were significantly higher in the endometrium in ewes that had been given a 5 day oxytocin infusion than in control animals (556 and 262 fmol mg-1 protein, respectively: geometric means from ANOVA, P < 0.001), whereas myometrial receptor concentrations were not affected (113 and 162 fmol mg-1 protein, respectively). We conclude that the previously reported delay in luteal development caused by oxytocin infusion (Wathes et al., 1991) is not due to the inhibition or delay of ovulation, but must instead occur via a direct influence on the developing corpus luteum.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of oxytocin infusion on secretion of progesterone and luteinizing hormone and the concentration of uterine oxytocin receptors during the periovulatory period in cloprostenol-treated ewes. 133 45

Human fetal membranes, taken from 30 patients submitted to caesarean section during the final stages of gestation and labor, were examined in order to evaluate the presence and characteristics of the oxytocin receptor. The presence of oxytocin receptors in human fetal membranes, both in the amnion and in the chorion-decidua, was demonstrated in this study. The receptor binding to oxytocin showed a significant increase during early and advanced labor compared with before the onset of labor. When the pre-labor level was taken as the normalized form (control = 100) the increase with respect to the control (10 cases) for the amnion in early labor (2.27 times +/- 0.11, mean +/- SEM, P less than 0.001, 10 cases) and in advanced labor (2.53 times +/- 0.15, 10 cases, P less than 0.001) was highly significant. In the chorion-decidua the increase was 1.61 times +/- 0.09, P less than 0.001 in early labor and 1.66 times +/- 0.19, P less than 0.001 in advanced labor. Scatchard analysis showed a single receptor site for oxytocin in amnion and chorion decidua. The dissociation constant (Kd) did not change during the various stages of labor; the mean values found were 0.228 +/- 0.02 (mean +/- SEM) nM in the amnion and 0.193 +/- 0.03 nM in the chorion-decidua respectively. These findings suggest that human fetal membranes are target organs for oxytocin and that they might play a role in the onset of labor through an increase of receptor binding.
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PMID:Oxytocin receptor in human fetal membranes at term and during labor. 215 53

Oxytocin at a physiological concentration stimulated the immediate release of free arachidonic acid from dispersed human decidual cells in a perfusion system. This indicates that oxytocin activates phospholipase(s) thus enhancing prostaglandin synthesis. The effect of oxytocin on the release of [3H]-arachidonic acid from decidual cells of women in labor was significantly greater (1036 +/- 207, mean dpm +/- SEM, n = 23) than from those of women not-in-labor (505 +/- 121 dpm, n = 12) or with endometrial cells of non-pregnant women (711 +/- 210 dpm, n = 18), and correlates well with reported oxytocin receptor concentrations in these tissues. These new findings are consistent with a role for endogenous oxytocin in stimulating prostaglandin synthesis at the onset of parturition.
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PMID:Oxytocin stimulates the release of arachidonic acid and prostaglandin F2 alpha from human decidual cells. 284 Jun 90

Explanted endometrial tissue from ovariectomized ewes that had received hormone replacement to mimic the luteal phase released platelet-activating factor (PAF) into medium in vitro. On Day 14, 310.1 (261-2185), and on Day 15, 424.4 (14.1-590.7) pg PAF (median 25th-75th percentile; p > 0.05) was released per 100 mg endometrial tissue after a 20-min incubation. A regulatory and final enzyme in the PAF biosynthetic pathway, lysoPAF:acetyltransferase, was also present with a specific activity of 0.533 +/- 0.124 pmol acetate/50 micrograms protein/30 min in Day 14 endometrial tissue and 0.810 +/- 0.468 in Day 15 tissue (mean +/- SEM; p > 0.05). PAF:acetylhydrolase, the metabolic enzyme regulating PAF's half-life, was present in uterine luminal washings, with a specific activity of 3.78 +/- 1.37 nmol acetate released/min/mg protein on Day 14 and 3.41 +/- 0.34 on Day 15 (mean +/- SEM; p > 0.05). Intrauterine infusion of 50-400 micrograms PAF caused a dose-dependent release of prostaglandin (PG) F2 alpha (measured as venous 14-dihydro-15-keto-prostaglandin F2 alpha, PGFM) within 10 min on Days 13-15. The enantiomeric form of PAF was significantly less effective in inducing a rise in venous PGFM. WEB 2086 is reported to be a competitive receptor antagonist for PAF, but a 10-fold excess of WEB 2086 failed to inhibit PAF-induced release of PGFM. It was observed that this dose of WEB alone induced PGFM release, suggesting that in this model this agent may not work as a true competitive antagonist. Repeat challenges at intervals of 0, 90, and 120 min with either 200 micrograms PAF or micrograms oxytocin resulted in a marked tachyphylaxis of response by the third challenge. This desensitization after repeated PAF challenge suggests a specificity of its actions. Infusion of 200 micrograms PAF on Day 14 or 15 at five 60-min intervals resulted in a tachyphylaxis such that by the fourth and fifth challenges, essentially no response was observed. The tachyphylaxis that was induced by four repeat challenges with PAF had no apparent effect on the capacity of the uterus to respond to a fifth challenge with oxytocin. Thus, PAF and oxytocin both caused homologous desensitization of their own capacity to mobilize uterine PGF2 alpha, but PAF did not cause heterologous desensitization of the response to oxytocin. This failure of heterologous desensitization suggests differences in the mechanism of action of the two ligands. Kinetic binding studies showed that PAF did not compete for the oxytocin receptor in vitro. This result demonstrated that the ovine endometrium produces PAF and responds to it by the release of PGF2 alpha in situ. The dynamics of the response elicited by PAF were similar to those of oxytocin, yet the two mediators apparently act separately. PAF may be a modulator of PGF2 alpha release by the ovine uterus during the luteal phase.
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PMID:Ovine endometrium synthesizes and releases platelet-activating factor, which can cause the release of prostaglandin F2 alpha by the uterus in situ. 878 86

The oxytocin receptor antagonist [1-deamino-2-D-Tyr-(OEt)-4-Thr-8-Om]-oxytocin (Atosiban) is a specific antagonist of both mesotocin- and oxytocin-induced myometrial contractions in late pregnant tammars in vitro. Continuous intravenous infusion of Atosiban (1 mg kg-1 day-1) for 3 or 7 days from day 24 of the 26.5 day gestation significantly delayed births. In both the 3 day and 7 day infusion groups, all 15 control animals were pregnant and gave birth within the normal time (day 26.75 +/- 0.20, mean +/- SEM), during the infusion of saline. The neonates weighed 387 +/- 8 mg. Deliveries were observed in 15 Atosiban-treated animals significantly (P < 0.05) later than in the controls (day 27.85 +/- 0.19; neonate weight 413 +/- 9 mg). All pouch young were successfully suckled, even in the continued presence of Atosiban. Baseline plasma concentrations of the prostaglandin F metabolite (PGFM) in pregnant tammars were < 200 pg ml-1. A surge in plasma PGFM occurred at birth (811 +/- 116 pg ml-1), followed by a rapid fall to baseline concentrations within 1 h after birth. This was observed both in saline- and in Atosiban-treated animals that gave birth during the observation period, and did not differ significantly between the treatment groups. Plasma progesterone concentrations in the control and the Atosiban-treated animals showed the normal pattern of luteolysis immediately after birth. Thus, infusion of an oxytocin receptor antagonist at the end of gestation delays birth, the peripartum surge in prostaglandin release, and the fall in progesterone, suggesting that mesotocin is an important part of the hormonal cascade associated with delivery in this marsupial.
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PMID:Infusion with an oxytocin receptor antagonist delays parturition in a marsupial. 895 39

The aim of this study was to evaluate the renal vascular effects of oxytocin in Sprague-Dawley rats and in Brattleboro heterozygous or homozygous rats, the latter being genetically deficient in vasopressin synthesis. Studies were performed in vitro, in the isolated kidney perfused in an open circuit with a Tyrode's solution. Oxytocin induced a concentration-dependent renal vasoconstriction in Sprague-Dawley rats, at rather high concentrations (EC50=170+/-39 nM, mean +/- SEM, n=6) with a maximum response amounting to 44% of that elicited by vasopressin (increase in renal vascular resistance: 11.5+/-0.9 mmHg min ml(-1) vs. 26.2+/-2.2 mmHg min ml(-1)). Oxytocin-evoked renal vasoconstriction was abolished by SR 49059, a selective vasopressin V1A receptor antagonist (10 nM), but not by d(CH2)5[Tyr(Me)2,Thr4,Orn8,Tyr-(NH2)9] vasotocin, an oxytocin receptor antagonist (10 nM). In the presence of SR 49059, oxytocin did not induce renal vasorelaxation. Oxytocin induced renal vasoconstriction in Brattleboro homozygotes and heterozygotes (EC50=59+/-12 nM and 262+/-110 nM; Emax=7.8+/-1.1 mmHg min ml(-1) and 6.9+/-0.4 mmHg min ml(-1), n=5 respectively) with characteristics similar as observed in Sprague-Dawley rats concerning partial agonist activity, low potency and antagonism by SR 49059. Responsiveness to vasopressin did not differ in Brattleboro homozygotes and heterozygotes (EC50 approximately 0.25 nM) and was similar as we reported in Sprague-Dawley rats. These findings indicate that high concentrations of oxytocin induce renal vasoconstriction in the rat by activating vasopressin V1A receptors. The low agonist activity makes it unlikely that oxytocin can substitute functionally for vasopressin at the renal vascular V1A receptor in Brattleboro homozygous rats which are deficient in endogenous vasopressin.
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PMID:High concentrations of oxytocin cause vasoconstriction by activating vasopressin V1A receptors in the isolated perfused rat kidney. 1133 Mar 29

The hormonal system for induction of term and preterm labour is not fully understood. Therefore, we investigated myometrial gene expressions for neurohypophyseal hormones and their receptors, prostaglandin F(2alpha) and ovarian steroid receptors in women delivered by Caesarean section. Myometrial tissue for real time PCR was collected from 39 women delivered at term before and after the onset of labour and preterm. Women delivered electively at term had significantly higher oxytocin receptor mRNA expressions (2.52 +/- 0.37 oxytocin receptor/actin; median +/- SEM) than those delivered with ongoing labour at term (1.01 +/- 0.34; p = 0.015) and those at preterm (1.08 +/- 0.25; p = 0.004). Sub-analyses revealed that the difference at term pregnancies solely was related to patients receiving oxytocin during labour (p = 0.007). These patients had higher oxytocin peptide mRNA levels than those without labour at term (p = 0.009). PGF(2alpha) receptor mRNA concentrations were 27.80 +/- 3.55, 11.46 +/- 2.87 and 19.54 +/- 5.52 PGF receptor/actin, respectively, for the groups. Women without labour at term had higher concentration than those with labour (p = 0.005). Our results suggest that oxytocin, its receptor and the PGF(2alpha) receptor are involved in the regulation of labour through a paracrine mechanism.
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PMID:Myometrial oxytocin receptor mRNA concentrations at preterm and term delivery - the influence of external oxytocin. 1934 9