Inhibition of progesterone synthesis in placenta by administration of dexamethasone to pregnant rats

Abstract

Glucocorticoid receptors have been detected in placenta from several species, including the rat, although the biological function of corticoids is unknown in placenta from the latter species. The present experiments examined the effect of glucocorticoid treatment on placental progesterone biosynthesis from endogenous precursors by incubated basal zone trophoblast and labyrinthine zone of placentas from adrenalectomized-ovariectomized rats at the end of pregnancy. It was found that a higher proportion of synthesized progesterone was retained in the tissue than that released into the incubation medium. Treatment of rats on the 17th–18th day of pregnancy with 10μg/ml of dexamethasone in the drinking saline for 3 days, produced a significant inhibition of progesterone detected in tissue and medium of incubated placental zones. In vitro addition of dexamethasone (10 −4 M) was also effective in reducing progesterone in the placental zone studied (LZ). Serum progesterone of intact rats was in the range of rats near parturition (approx 25ng/ml) and dropped to almost undetectable levels in rats with adrenalectomy and ovariectomy, with or without dexamethasone treatment, suggesting that in late pregnancy the rat placenta does not contribute significantly to circulating levels of progesterone. This glucocorticoid effect could not be extended to estrogens, as we, in accord with the work of other groups, failed to detect estrogen synthesis in rat placenta. It is suggested that a function for glucocorticoid receptors in rat placenta may be the inhibition of local progesterone production.