Prolactin inhibits oocyte release after gonadotropin stimulation in the rat: putative mechanism involving ovarian production of beta-endorphin and prostaglandin.

Objective: To evaluate whether prolactin (PRL) is able to inhibit ovulation induced with exogenous gonadotropins in the rat and whether this effect could be mediated by the ovarian production of beta-endorphin, prostaglandin, and nitric oxide (NO).

Design: Controlled in vivo and in vitro experiments.

Setting: Academic research laboratories.

Animal(s): Immature female rats undergoing ovulation induction with equine gonadotropins and hCG.

Intervention(s): Prolactin (100 or 200 microg), PRL + the opioid antagonist naloxone (200 microg each), or placebo were injected SC 4 hours after hCG administration for ovulation induction. In the in vitro experiments, isolated preovulatory ovaries were incubated with or without PRL in a final concentration of 100 or 200 ng/mL.

Main Outcome Measures(s): Number of oocytes ovulated in vivo, ovarian beta-endorphin, PGE(2) and NO(2)(-)/NO(3)(-) release, and NO synthase activity in vitro.

Result(s): Prolactin reduced significantly the number of oocytes ovulated at the doses of 100 and 200 microg, and this effect was partially reversed by naloxone administration together with 200 mug PRL. PRL also induced a twofold increase in the ovarian release of beta-endorphin and a threefold decrease in the ovarian production of PGE(2). Ovarian NO synthase activity and the concentrations of NO(2)(-)/NO(3)(-) in the incubation medium were not modified by PRL.

Conclusion(s): Prolactin is able to reduce the number of oocytes released and modulate ovarian beta-endorphin and PGE(2) release, which may account for its peripheral anovulatory effects. This local effect of PRL could interfere in the process of ovulation induction by exogenous gonadotropins.