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  • Title: Antifertility actions of the progesterone antagonist RU 486 include direct inhibition of placental hormone secretion.
    Author: Das C, Catt KJ.
    Journal: Lancet; 1987 Sep 12; 2(8559):599-601. PubMed ID: 2887889.
    Abstract:
    the antifertility effects of the potent antiprogestin RU 486 (mifepristone) during early pregnancy have been attributed to its blockade of progesterone receptors in the endometrium. Studies in cultured syncytiotrophoblasts have revealed an additional action of RU 486 at the placental level, where it impairs the production of human chorionic gonadotropin (hCG), human placental lactogen (hPL), and progesterone. RU 486 (10 nmol-10 mumol/l) attenuated the production of all three placental hormones, in a dose-related manner, and its effects on hCG and hPL were reversed by addition of exogenous progesterone. The specific inhibitory effects of RU 486 on placental hormone secretion indicate that its antifertility actions are attributable to competitive inhibition of progesterone action in the trophoblast as well as in the endometrium. Synthetic mifepristone (RU 486) is a potent progesterone antagonist that inhibits the uterine actions of progesterone and has pronounced antifertility effects in rodents. It acts by competitive antagonism of progesterone at the receptor level, with blockade of its biologic effects in reproductive tissues including endometrium and cervix, and at the hypothalamic-pituitary level. When administered to women during early pregnancy, RU 486 causes vaginal bleeding followed by expulsion of the placenta 4-5 days later. RU 486 also decreases or abolishes the daily increase in urinary human chorionic gonadotropin (hCG) that is characteristic of early pregnancy. This study investigated this aspect of the action of RU 486 in cultured placental cells. The cytotrophoblasts cultured from human term placentae differentiated into syncytiotrophoblasts within 48 hours and produced increasing amounts of hCG, human placental lactogen (hPL), and progesterone. The effects of RU 486 on placental hormone secretion were evaluated in cells cultured for an additional 24 hours. RU 486 caused dose-dependent inhibition of hCG, hPL, and progesterone production. The concentrations of the antiprogestin that achieved this effect were in the range of the plasma levels required for its contragestive actions in women. The effects of RU 486 on hCG and hPL were reversed by addition of exogenous progesterone. The specific inhibitory effects of RU 486 on placental hormone secretion indicate that its antifertility actions are attributable to competitive inhibition of progesterone action in the trophoblast as well as in the endometrium.
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