Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Indomethacin administration in late pregnancy prolonged gestation in caged rhesus monkeys and inhibited premature labour and postponed delivery in chronically catheterized monkey fetuses. Chronic indomethacin treatment was associated with a reduction in the urinary excretion of a prostaglandin metabolite, a potent inhibitory effect on myometrial cyclic AMP phosphodiesterase, and severe oligohydramnios in pre-term and post-term fetuses. Experimental anencephaly (functional hypophysectomy) of the rhesus fetus results in lowered concentrations of maternal oestradiol and loss of the precise control of gestational length, with 40% of fetuses delivering beyond term. Corticotropin (ACTH) infused into the fetus results in raised concentrations of fetal and maternal cortisol, progesterone and oestrogens. Progesterone concentrations in peripheral blood apparently have little bearing on uterine quiescence in the rhesus monkey, since the concentrations of progesterone in maternal and fetal blood vary directly with uterine activity. The results of chronic infusion of corticotropin in the fetal monkey support the theory that in the monkey parturition is mediated by increased oestrogen production by the fetoplacental unit and by a rise in the concentrations of oestrone and prostaglandin in the amniotic fluid.
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PMID:Endocrine and pharmacological factors which influence the onset of labour in rhesus monkeys. 20 94

Fetal plasma growth hormone concentrations were measured in 15 pregnant ewes over the last 5 days before delivery. In five chronically catheterized pregnant ewes that underwent spontaneous vaginal delivery 146 +/- 2 days (mean +/- SD) of gestation, fetal plasma growth hormone concentrations fell from 124.6 +/- 44.1 ng X ml-1 5 days before delivery to 35.2 +/- 31.3 ng X ml-1 at delivery. In three fetuses in which premature delivery was induced by the infusion of cortisol to the fetus at 128 days of gestation, fetal plasma growth hormone levels fell from 195 +/- 19.1 ng X ml-1 to 70.7 +/- 25.5 ng X ml-1 over the last 5 days of intrauterine life. In seven fetuses in which premature delivery was induced with infusion of synthetic adrenocorticotropin to the fetus beginning at 120 or 130 days of gestation, the fetal plasma growth hormone level did not fall (175.6 +/- 75.7 to 158.9 +/- 60.1 ng X ml-1). Fetal plasma cortisol concentrations at delivery were significantly higher in the cortisol-infused fetuses (214 +/- 38.4 ng X ml-1) than in both control (94.4 +/- 33.7 ng X ml-1) and adrenocorticotropic hormone-infused fetuses (94.5 +/- 31.9 ng X ml-1). The fall in the fetal plasma growth hormone level in cortisol-induced fetuses may be due to the higher fetal plasma cortisol concentrations achieved in the cortisol-infused compared with the adrenocorticotropic hormone-infused fetuses in which no comparable decrease in growth hormone was observed. These findings suggest that there are significant differences in the fetal response to various experimental regimens used for the induction of premature labor in the sheep.
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PMID:Plasma growth hormone concentration in the chronically catheterized ovine fetus during spontaneous term delivery and premature delivery induced by continuous intravascular infusion of low doses of adrenocorticotropin or cortisol to the fetus. 300 21

Amniotic fluid beta-endorphin (beta-EP) and beta-lipotropin (beta-LPH) were measured by radioimmunoassay after silicic acid extraction and gel chromatographic separation of the two peptides in uncomplicated second-trimester and term pregnancies, in diabetic patients at term, and in pregnancies complicated by Rh-isoimmunization, premature labor, and intrauterine growth retardation. Furthermore, the lecithin/sphingomyelin (L/S) ratios as well as the dehydroepiandrosterone sulfate (DHEA-S) and cortisol levels were determined in most of the amniotic fluid specimens. Both the mean (+/- SE) beta-EP (65.3 +/- 9.1 fmol/ml) and beta-LPH (150 +/- 15.8 fmol/ml) concentrations were significantly higher in the 20 patients with normal pregnancies of 16 to 21 weeks' duration than those found in 21 patients with uncomplicated term pregnancies of 38 weeks' gestation, averaging 42.6 +/- 6.0 and 80.1 +/- 10.7 fmol/ml, respectively. The mean amniotic fluid beta-EP and beta-LPH concentrations measured in the latter subjects were similar to those observed in 23 diabetic patients with otherwise uncomplicated term pregnancies. The mean amniotic fluid beta-EP and beta-LPH levels found in the limited number of patients with Rh-isoimmunization (N = 9), premature labor (n = 8), and intrauterine growth retardation (n = 5) with pregnancies of 24 to 36, 24 to 36, and 34 to 38 weeks' gestation, respectively, were not significantly different from the mean amniotic fluid beta-EP and beta-LPH concentrations of uncomplicated term pregnancies. In all patients but those with Rh-isoimmunization, beta-EP concentrations exhibited a positive correlation with beta-LPH levels. However, the molar beta-LPH:beta-EP ratio was significantly lower at term than during the early second trimester. Neither beta-EP nor beta-LPH correlated with the amniotic fluid L/S ratio and only beta-LPH exhibited a significant inverse correlation with amniotic fluid DHEA-S. The latter was significantly higher in uncomplicated term than second-trimester pregnancies. These results confirm that immunoassayable beta-EP is present in amniotic fluid and declines toward term. These data demonstrate that immunoassayable beta-LPH is present in amniotic fluid and show a more pronounced decrease toward the end of pregnancy than beta-EP. Neither peptide, at least on account of the amniotic fluid levels, appears to be associated with fetal maturation. The physiologic significance of amniotic fluid beta-EP and beta-LPH and their possible role as markers of fetal response to stress remain to be elucidated.
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PMID:Amniotic fluid beta-endorphin and beta-lipotropin concentrations during the second and third trimesters. 630 49

Preterm labor is the final common pathway after several potential insults to the uterus or fetus. The preterm labor syndrome may be precipitated by several different pathophysiologic events, including intrauterine infection, uterine ischemia, uterine overdistention, hormonal disturbances, and other problems. Intrauterine infections (both clinically evident and subclinical) are associated with increased amniotic fluid concentrations of proinflammatory cytokines, and gestational tissues and the fetus are potential sources of these cytokines. In addition to culture-proven intrauterine infection, there may be an "intrauterine inflammatory response syndrome" that could account for cases of preterm labor in which no infectious organism can be identified. Because the immunologic and endocrinologic systems regulate each other extensively, there is potential for corticotropin-releasing hormone to regulate inflammatory responses and vice versa. The cytokine interleukin 1 stimulates production of corticotropin-releasing hormone, and corticotropin-releasing hormone in turn regulates cytokine production by immune effector cells. Because maternal stress is associated with preterm birth, abnormalities in the regulation of corticotropin-releasing hormone and the production of inflammatory cytokines may be a mechanism that could form the pathophysiologic basis for this association.
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PMID:Immunoendocrinology of preterm labor: the link between corticotropin-releasing hormone and inflammation. 991 28

The fundamental process of implantation involves a series of steps leading to effective cross-talk between invasive trophoblast cells and the maternal endometrium. The molecular interactions at the embryo-maternal interface during the time of blastocyst adhesion and subsequent invasion are not fully understood. Embryonic trophoblast and maternal decidual cells produce corticotropin-releasing hormone (CRH) and express Fas ligand (FasL), a proapoptotic cytokine. Fas and its ligand are pivotal in the regulation of immune tolerance. Trophoblast and decidual CRH play crucial roles in implantation, as well as in the anti-rejection process that protects the fetus from the maternal immune system, primarily by killing activated T cells through Fas-FasL interaction. The potential use of CRH antagonists is presently under intense investigation. CRH antagonists have been used experimentally to elucidate the role of CRH in blastocyst implantation and invasion, early fetal immunotolerance, and premature labor.
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PMID:Reproductive corticotropin releasing hormone, implantation, and fetal immunotolerance. 1794 93