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)

Treatment of pregnant rats with 1 mg indomethacin/kg twice daily i.m. beginning on Day 20 delayed the onset of parturition by about 21 hr and prolonged the duration of spontaneous parturition by 4 hr. Plasma progesterone and oestradiol levels were determined in daily samples of peripheral blood, and uterine contractions were recorded before and during parturition by means of small, chronically implanted intrauterine balloons which were connected to pressure transducers via fluid-filled catheters. Indomethacin treatment did not inhibit or suppress spontaneous or oxytocin-induced contractions, which were of the same intensity in indomethacin-treated as in control rats. Parturition was induced with oxytocin in the same proportion of treated and control rats, but its induction was not successful in treated rats until 1 day later than in control rats, but its induction was not successful in treated rats until 1 day later than in controls. The onset of parturition was always related to the plasma progesterone level, which declined at a slower rate in indomethacin-treated than in control rats, reaching baseline values approximately 1 day later in the treated animals. The appearance of 20alpha-hydroxysteroid dehydrogenase in the CL of pregnant rats normally occurs on Day 21 of gestation, but activity was not observed until about 1 (0-3) day later in the indomethacin-treated rats, indicating that luteolysis was retarded. Prostaglandin F-2alpha infusions given on Day 21 reversed the effects of indomethacin treatment on plasma progesterone, luteal 20alpha-hydroxysteroid dehydrogenase activity and the timing and duration of parturition, and reduced the high perinatal mortality associated with indomethacin treatment, suggesting that the effects of indomethacin were related to its inhibitory action on prostaglandin synthetase activity. It is concluded that, in rats, indomethacin exerts its effects on parturition through inhibition of luteal regression which was significantly retarded but not prevented, and that indomethacin does not have a direct effect on myometrial contractility.
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PMID:The effect of indomethacin on uterine contractility and luteal regression in pregnant rats at term. 103 79

During reproductive processes, prostaglandin (PG) E(2) (PGE(2)) and PGF(2alpha) play important roles in which they often exert opposite effects. At the time of recognition of pregnancy in vivo, PGF(2alpha) is recognized as the luteolytic factor in ruminants and in most species including human, whereas PGE(2) may exert a luteoprotective action. We have previously demonstrated that recombinant interferon-tau (rIFN-tau), the embryonic signal responsible for recognition of pregnancy in ruminants, stimulated in vitro the production of PGE(2) and prostaglandin-endoperoxide synthase 2 (Ptgs2; also called cyclooxygenase-2) gene expression in both epithelial and stromal endometrial cells. Since PGE(2) is the major prostaglandin produced by stromal cells, the effect on Ptgs2 could explain the increase in PGE(2) output. At high concentrations, however, recombinant ovine (ro) IFN-tau acts on epithelial cells by changing the primary PG produced from PGF(2alpha) to PGE(2). This change in the primary PG produced could be explained by a decrease in PGF synthase (PGFS) activity or an increase in PGE synthase activity, or by modulation of a putative PGE(2)-9-ketoreductase, which converts PGE(2) into PGF(2alpha). Therefore, we have investigated the regulation of the mRNAs for PGFS and PGE(2)-9-ketoreductase (9K-PGR), two enzymes that lead to the production of PGF(2alpha). Others have described 9K-PGR activity in uterus, ovaries, kidney, and liver of different species and have established that this enzyme could possess both 9K-PGR and 20alpha-hydroxysteroid dehydrogenase (20alpha-HSD) activity. Some have concluded that 9K-PGR and 20alpha-HSD are identical enzymes. Using primers sequences chosen from homologous nucleotide sequences of published rabbit 20alpha-HSD/9K-PGR and rat 20alpha-HSD cDNAs, a 317-base pair (bp) fragment was amplified by reverse transcription-polymerase chain reaction (RT-PCR), cloned, and sequenced. Homologies of 83% and 78% were found with rabbit and rat 20alpha-HSD, respectively. The presence of 20alpha-HSD/9K-PGR and prostaglandin F synthase (PGFS) mRNA expression was studied semiquantitatively in cultured epithelial cells using RT-PCR. Stimulation of cells with roIFN-t resulted in a biphasic response, an inhibition of PGF(2alpha) production at low dose (1 ng/ml) and a stimulation of PGE(2) at high dose (10 microg/ml). The increase of PGE(2) was accompanied by reduced 9K-PGR and PGFS mRNA gene expression. The effect of oxytocin (OT) was also studied, and the presence of OT had no effect on either 9K-PGR or PGFS gene expression. The 20alpha-HSD/9K-PGR transcript was also detected in other bovine tissues at different intensity (liver > kidney > testis > ovaries). We believe that the 9K-PGR and PGFS can be key enzymes in the regulation of specific PGs in the endometrium during the periimplantation period.
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PMID:Detection and regulation of the messenger for a putative bovine endometrial 9-keto-prostaglandin E(2) reductase: effect of oxytocin and interferon-tau. 1061 Oct 76