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Journal of Clinical Endocrinology & Metabolism, Vol 55, 213-218, Copyright © 1982 by Endocrine Society

ARTICLES

Effects of dibutyryl adenosine 3',5'-monophosphate, luteinizing hormone- releasing hormone, and aromatase inhibitor on simultaneous outputs of progesterone, 17 beta-estradiol, and human chorionic gonadotropin by term placental explants

RV Haning Jr, L Choi, AJ Kiggens, DL Kuzma and JW Summerville

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, 17 beta- 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 17 beta-estradiol remained constant during the course of the incubation. The addition of 67 micrograms/ml LDL cholesterol had no effect on the basal output of 17 beta-estradiol, progesterone, or hCG. The addition of 4 micrograms/ml DHEAS increased 17 beta-estradiol output 20-fold, but did not affect the outputs of hCG or progesterone. The addition of 1.6, 3.2, or 6.4 micrograms/ml LRH had no effect on the output of progesterone or 17 beta-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 17 beta-estradiol output in medium supplemented with DHEAS. Aromatase inhibitor decreased both 17 beta- 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 17 beta-estradiol, but the effect on hCG was direct and not due to the decrease in 17 beta-estradiol.


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