Prostaglandin F Mediation of the Inhibitory Effect of Estrogen on the Corpus Luteum of the Rhesus Monkey*

Estrogen administration during the luteal phase of the menstrual cycle has been shown to be luteolytic; however, the exact mechanism is inknown. Since estrogen is known to inhibit LH release, cause a release of prostaglandin F2α(PGF) and act directly on the corpus luteum to lower progesterone (P), the possibility exists that estrogen's mechanism of action is mediated by any one or all of these effects. We have investigated the acute effects of 17β-estradiol (E) administration on LH release, on progesterone secretion by the corpus luteum, and on the release of PGF from the primate ovary. Normally cycling monkeys were selected on days 19–20 of the cycle (5–7 days after the periovulatory estradiol surge). Under general anesthesia, the ovarian vein ipsilateral to the corpus luteum was cannulated, and blood was collected on ice at 20-min intervals for 4 h [1 h before treatment (control) and 3 h during treatment]. The animals were randomly divided into four experimental groups: 1) control (vehicle treatment), 2) estradiol (1 ng/min iv for 3 h), 3) estradiol- indomethacin (15 ng/kg indomethacin im, followed by estradiol, as above), 4) indomethacin (15 ng/kg im, followed by estradiol-vehicle). A peripheral vein sample was taken at the start and at the conclusion of each experiment, and the blood was analyzed for LH, PGF, P, and E by RIA. Vehicle treatments had no effect on ovarian and peripheral LH, PGF, P, or E. Estradiol infusion lowered ovarian and peripheral P and raised PGF without any change in LH. Indomethacin blocked the P decrease caused by estradiol without any significant change in LH values. The results of this study suggest that the mechanism of estradiol-induced luteolysis in the rhesus monkey is mediated through intraovarian PGF.