Steroid hormones modulate the release of immunoreactive gonadotropin-releasing hormone from cultured human placental cells.

The aim of the present study was to evaluate whether steroid hormones or opiate receptor agonists participate in the mechanisms regulating the release of immunoreactive GnRH (irGnRH) from cultured human placental cells. No significant changes in irGnRH concentrations were found in the culture medium after 48-h incubation of estradiol, estriol, or progesterone. Both estriol and estradiol augmented, while progesterone decreased, the irGnRH release induced by 8-bromo-cAMP. The stimulatory effect of estriol or estradiol was reversed by the concomitant addition of progesterone. The secretagogue effect of activin on irGnRH release from cultured placental cells was increased by the presence of estriol and reduced by the addition of progesterone. The action of estriol was counteracted by both tamoxifen, an estrogen antagonist, and progesterone. The inhibitory effect of progesterone was completely reversed by RU 486, a specific receptor antagonist. The addition of morphine, methionine-enkephalin, or UP50, 488H which preferentially bind mu-, delta-, and kappa-opiate receptors, respectively, did not decrease basal irGnRH release from cultured human placental cells. However, both morphine and UP50, 488H significantly inhibited 8-bromo-cAMP-induced GnRH release. The present results showed that steroid hormones and opiate receptor agonists influence irGnRH release from human cultured cells, suggesting that local interaction between steroids and peptides modulates irGnRH release from human placenta.