Prostaglandins were injected either intravenously, intraventricularly, or into the anterior pituitary gland to evaluate their possible participation in the control of gonadotropin release. Their effect on plasma LH and FSH was determined by radioimmunoassay. Intravenous injection of prostaglandin E2 (PGE2) produced a slight increase in plasma LH but not FSH in ovariectomized animals. Prostaglandin E1 (PGE1), PGFlα and PGF2α were ineffective. Third ventricular (3rd V) injections of PGE2 induced a marked increase in plasma LH in ovariectomized rats. The increase was much greater than that observed following iv injection, and PGE1, Flα or F2α were ineffective. A slight increase in plasma FSH also followed 3rd V injection of PGE2. Ovariectomized animals were injected SC 48 hr prior to the experiment with estradiol benzoate (10 µg) to sensitize the pituitary gland to the gonadotropin-releasing factor(s). In these animals 3rd V injections of PGE2 produced a dose-related increase in plasma LH. In addition, a significant increase was also obtained with PGE1. The other prostaglandins and the diluent were again ineffective. Intrapituitary injections of PGE2 and E1 were ineffective in ovariectomized animals but PGE2 produced a small increase in LH in the estrogenprimed rats. The results indicate that PGE2 and to a lesser extent PGE1 have a specific effect in stimulating the release of LH by the adenohypophysis. The principal site of action appears to be on the central nervous system (CNS) with another less important site on the anterior pituitary itself. The findings suggest that PGE2 and possibly PGE1 are involved in neural control of pituitary gonadotropin release.
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