CHANGES IN FETAL PLASMA CORTICOTROPIN-RELEASING HORMONE DURING ANDROSTENEDIONE-INDUCED LABOR IN THE RHESUS-MONKEY - LACK OF AN EFFECT ON THE FETAL HYPOTHALAMO-PITUITARY-ADRENAL AXIS

Androstenedione infusion to pregnant monkeys leads to premature labor and Live delivery. Androstenedione-induced labor also increased placen tal CRH messenger RNA and peptide to concentrations observed at term i n pregnant monkeys. Placental CRH may modulate fetal pituitary-adrenal function during pregnancy in primates. This study tested the hypothes is that androstenedione-induced premature delivery in pregnant monkeys results from androstenedione-induced increases in placental CRH, whic h stimulate premature activation of the fetal pituitary-adrenal axis. The hypothesis was tested by comparing fetal umbilical vein (FUV) plas ma CRH, ACTH, dehydroepiandrosterone sulfate, and cortisol concentrati ons at cesarean section in fetuses from mothers undergoing spontaneous , term labor (group I), with those in fetuses from mothers undergoing androstenedione-induced, premature labor (group IE) and with those fro m mothers not in labor (group III). In addition, gestation-related cha nges in maternal plasma CRH concentrations were investigated, and CRH immunoactivity was characterized by Sephadex G50 chromatography in poo led maternal plasma extracts. FUV CRH concentrations were similarly el evated in group I and group II fetuses, compared with group III fetuse s. Despite similar FUV blood gases in all fetuses, FUV ACTH and dehydr oepiandrosterone sulfate concentrations were higher in group I fetuses than in group II or group III fetuses. The majority of CRH immunoacti vity coeluted with synthetic human CRH. Maternal plasma CRH concentrat ions showed a modest increase with gestation in the rhesus monkey. The se data: 1) demonstrate that androstenedione treatment of pregnant mon keys at 0.8 of gestation elevates fetal plasma CRH to similar concentr ations measured at term; 2) do not support the hypothesis that androst enedione-induced delivery in the monkey results from premature activat ion of the fetal pituitary-adrenal axis by placental CRH; but 3) do su pport a role for activation of the fetal hypothalamo-pituitary-adrenal axis in association with spontaneous term labor in the monkey; and 4) demonstrate important interprimate species differences in maternal CR H physiology.