Two experiments were conducted to determine the effects of pregnenolone (P5), cyclic adenosine monophosphate (cAMP), and human chorionic gonadotropin (hCG) on porcine placental and endometrial production of progesterone (P4) and estrone (E1) in vitro at days 30, 60 and 90 of gestation. Placental P4 production increased between days 30 and 90 and was enhanced by the addition of P5. A further increase in placental P4 production occurred at days 30 and 90 due to cAMP supplementation. Addition of hCG failed to increase placental P4 production at any day. Placental E1 production in vitro was biphasic and mimicked the pattern seen in maternal plasma and fetal fluids. Placental E1 production in P5-supplemented medium was enhanced by the addition of cAMP at day 90. However, hCG supplementation reduced placental E1 production at day 90. Endometrial P4 and E1 production were similar to those of the placenta at day 30 of gestation. However, unlike placental steroidogenesis, endometrial hormone production remained relatively constant over the 3 days of gestation examined. Supplemental P5 enhanced endometrial P4 and E1 production. The overall magnitude of response to supplementation was considerably less in endometrial vs placental tissue. We conclude that both porcine placental and endometrial tissues are steroidogenically competent but that placenta is the far more active and responsive tissue. The mechanism controlling placental steroidogenesis apparently does not involve LH/hCG tropic stimulation, but cAMP is an effective intracellular second messenger.