<i>In Utero</i>Regulation of Rhesus Monkey Fetal Adrenals: Effects of Dexamethasone, Adrenocorticotropin, Thyrotropin-Releasing Hormone, Prolactin, Human Chorionic Gonadotropin, and α-Melanocyte-Stimulating Hormone on Fetal and Maternal Plasma Steroids*

Abstract

In utero regulation of primate fetal adrenal glands and their role in steroidogenesis were studied between days 125-143 of gestation (term, 167 days) in chronically catheterized rhesus monkeys. Changes in fetal and maternal plasma cortisol, progesterone, estrone, estradiol, and PRL were determined in response to infusion of dexamethasone into mothers and ACTH, TRH, PRL, hCG, or α-MSH into fetuses. Significant, (P < 0.01) differences between maternal and fetal concentrations were observed in control samples for estradiol and cortisol but not for estrone, progesterone, or PRL. Estradiol and cortisol levels were higher in the maternal than in the fetal circulation. Dexamethasone administration decreased (P < 0.05) maternal cortisol, estrone, and estradiol and fetal cortisol and estrone. Administration of ACTH to fetuses increased (P < 0.05) fetal cortisol, progesterone, and estrone. The level of fetal estradiol was relatively low and was not altered by dexamethasone or ACTH (P > 0.05). Despite continued suppression of the maternal adrenals with dexamethasone and a lack of ACTH transfer from the fetal to the maternal circulation, concentrations of maternal cortisol, estrone, and estradiol were also increased (P < 0.05). The concentrations of fetal cortisol and estrone and of maternal cortisol, estrone, and estradiol returned to predexamethasone control values during infusion of ACTH into fetuses. Administration of TRH to fetuses increased (P < 0.05) fetal and maternal PRL. The increase in the maternal circulation was considerably larger than that in the fetal circulation. Despite endogenous increases in fetal and maternal PRL produced by TRH or exogenous administration of PRL to fetuses, no significant changes (P > 0.05) occurred in fetal or maternal estrone, estradiol, progesterone, or cortisol during the 4-h infusion period. Likewise, infusion of hCG or a-MSH into fetuses did not alter fetal or maternal plasma steroid levels. These data indicate that 1) ACTH, but not PRL, hCG, or a-MSH, is an important regulator of rhesus fetal adrenals between days 125–143 of gestation; 2) rhesus fetal adrenals are involved in the biosynthesis of cortisol, progesterone, estrone, and estradiol; 3) fetal adrenals have the steroidogenic capacity to maintain fetal as well as maternal plasma levels of cortisol and estrogens; and 4) maternal:fetal concentration differences are present for cortisol and estradiol but not for progesterone, estrone, or PRL. We suggest that the placenta is primarily responsible for maintaining the steroid concentration differences.