Estradiol-Induced Luteal Regression in the Rhesus Monkey: Evidence for an Extraovarian Site of Action*

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Abstract
Studies were performed to test the hypothesis that estradiol is a physiologic luteolysin in the rhesus monkey and that it acts within the ovary containing the corpus luteum. Samples of peripheral blood were collected every 4 h and analyzed for various reproductive hormones to provide an index of the pattern of estradiol produced just before and during luteal regression, as monitored by serum progesterone concentration. After ovulation, serum estradiol rose to a midluteal phase plateau of 30–40 pg/ml, then rose again to nearly 70 pg/ml in the late luteal phase. The second increase in estradiol occurred after progesterone had begun to decline, suggesting that this latter rise does not initiate luteolysis. Evidence that the midluteal phase plateau in circulating estradiol might contribute to luteolysis was provided by the response to exogenous estradiol administered via small Silastic implants. Premature luteolysis was induced in 7 of 12 monkeys by sustained intraluteal delivery of a dose of estradiol which mimicked its midluteal phase plateau in peripheral serum. Serum LH was suppressed significantly below the control level only in those 7 monkeys in which premature luteolysis occurred. Further, sc delivery of the same amount of estradiol also induced premature luteolysis and depressed circulating LH, but it did so without producing an increase in the concentration of estradiol within the corpus luteum. Coupled with the observation that circulating LH in untreated monkeys declines as the midluteal phase plateau of estradiol is achieved, the foregoing observations are consistent with the hypothesis that a rising tide of estradiol contributes to luteolysis in the rhesus monkey by virtue of its well documented capacity to suppress LH secretion. Thus, while reinforcing the hypothesis that estrogens play some role in the luteolytic process of the rhesus monkey, our findings point toward a mechanism that includes a suppression of LH secretion.