Effects of dibutyryl cyclic AMP and gonadotropin-releasing hormone added prior to filter sterilization of the media and variation in oxygen partial pressure on output of human chorionic gonadotropin from term placental explants.

The effect of 2 mM dibutyryl cyclic AMP (dbcAMP) and 10 and 100 micrograms/ml gonadotropin-releasing hormone (GnRH) added prior to filter sterilization and of varying oxygen partial pressure (5, 20, and 95% oxygen) were evaluated using explants from each of 4 placentas on each of 6 days of culture. There were significant differences between placentas on days 1 and 2 of culture (both p less than 0.025), and day 4 (p less than 0.05), but there were no effects of GnRH or varying oxygen partial pressure on output of human chorionic gonadotropin under the conditions evaluated.

Interrelationships among human chorionic gonadotropin (hCG), 17 beta-estradiol, progesterone, and estriol in maternal serum: evidence for an inhibitory effect of the fetal adrenal on secretion of hCG.

In normal pregnancy, maternal serum hCG reaches a maximum concentration about 8-10 weeks after the last menstrual period and then decreases. To investigate the possibility that this decrease in hCG is produced by an inhibitory effect of steroids originating in the feto-placental unit, hCG, progesterone, 17 beta-estradiol, and estriol were determined by specific RIAs in 341 serum specimens obtained from 229 different pregnancies. Expressions for predicted hCG as a function of estimated trophoblastic mass and percent predicted hCG were determined to correct for the increase in hCG with increasing trophoblastic mass. The relationships between hCG and progesterone, 17 beta-estradiol, estriol, or estimated trophoblastic mass were not linear. Expression of the hCG data as percent predicted hCG produced linear relationships between hCG and each of the above steroids. Both hCG itself and percent predicted hCG were shown to have a negative regression on estriol (P less than 0.001) and a positive regression on progesterone (P less than 0.001), but not on 17 beta-estradiol (P greater than 0.05), in a multiple linear regression on all three steroids. These data suggest that hCG production is inhibited by a steroid originating in the fetal adrenal. This inhibitory effect plateaus in late pregnancy, allowing a minor late increase in hCG due to increasing trophoblastic mass.