Physiological role of prostaglandins in the induction of ovulation

It is concluded that indomethacin, under the conditions studied, does not block LH release, but exerts its anti-ovulatory action directly on the follicle: it prevents follicular rupture, but not ovum maturation, and prostaglandins are not indispensible for this action of LH.

Abstract

The administration of prostaglandin E2 at the dose levels of 0.7, 1.0 and 1.5 mg/rat on the afternoon of proestrus to adult rats in which the pre-ovulatory surge of LH was prevented by Nembutal induced ovum maturation in 58, 70 and 90% and ovulation in 42, 60 and 81% of the animals, respectively; the incidence of persistent uterine distension was reduced by the prostaglandin treatment, suggesting that ovarian progesterone secretion was stimulated. Injection of indomethacin, an inhibitor of prostaglandin synthesis, on its own at 14.30 on the day of proestrus (5 – 10 mg/rat) prevented follicular rupture in 78 – 89% of the animals, but maturation of the oocytes retained in the follicles was unimpaired. Concomitant treatment with indomethacin and Nembutal prevented both follicular rupture and ovum maturation. Administration of LH at a dose level adequate to induce ovulation in Nembutal-blocked rats (2.5 μg/rat), failed to overcome the indomethacin-induced block of ovulation, but prostaglandin E2 brought about follicular rupture in the majority of the indomethacin-treated animals. It is concluded that (i) indomethacin, under the conditions studied, does not block LH release, but exerts its anti-ovulatory action directly on the follicle: it prevents follicular rupture, but not ovum maturation; (ii) prostaglandins have an essential role in the mechanism by which LH brings about follicular rupture; (iii) though prostaglandin E2 is able to induce ovum maturation, prostaglandins are not indispensible for this action of LH.