Effects of Dibutyryl Adenosine 3',5'-Monophosphate, Luteinizing Hormone-Releasing Hormone, and Aromatase Inhibitor on Simultaneous Outputs of Progesterone, 17β-Estradiol, and Human Chorionic Gonadotropin by Term Placental Explants*

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Abstract
To contrast the effects of dibutyryl cAMP (dbcAMP) with those of LRH and to evaluate the effects of low density lipoprotein (LDL), dehydroepiandrosterone sulfate (DHEAS), and aromatase inhibitor (4-hydroxy-androst-4-ene-3,17-dione) on the output of hCG, β-estradiol, and progesterone, term human placental explants were maintained in culture for 6 days with daily changes of medium. The daily outputs of progesterone and hCG were observed to decrease while that of β-estradiol remained constant during the course of the incubation. The addition of 67 μg/ml LDL cholesterol had no effect on the basal output of 17β-estradiol, progesterone, or hCG. The addition of 4 μg/ml DHEAS increased β-estradiol output 20- fold, but did not affect the outputs of hCG or progesterone. The addition of 1.6, 3.2, or 6.4 μg/ml LRH had no effect on the output of progesterone or 17β-estradiol. LRH increased hCG output in Dulbecco's Modified Eagle's Medium with penicillin, streptomycin, insulin, and glucose alone, but not in the presence of added LDL or DHEAS, while dbcAMP (1, 2, and 4 mM) increased the output of hCG in all three media and decreased β- estradiol output in medium supplemented with DHEAS. Aromatase inhibitor decreased both β-estradiol and hCG outputs in a dose-dependent fashion, but it was without effect on the output of progesterone. Basal progesterone, basal hCG, and dbcAMP-stimulated hCG outputs were unaffected by the addition of LDL or DHEAS. Both LDL and DHEAS inhibited the stimulatory effect of LRH on the output of hCG. Aromatase inhibitor decreased the output of both hCG and 17β-estradiol, but the effect on hCG was direct and not due to the decrease in 17β-estradiol.