Circulating levels of steroids and chorionic gonadotropin during pregnancy in the rhesus monkey, with special attention to the rescue of the corpus luteum in early pregnancy.

Abstract

Circulating levels of progesterone and estrogen in the pregnant rhesus monkey are indistinguishable from those of the nonpregnant animal until 12 days after the LH peak, when the first significant rise in chorionic gonadotropin (RhCG) levels is noted concomitant with an abrupt elevation in progesterone levels (the corpus Iuteum rescue). Serum RhCG concentration rises rapidly (doubling time = 2 days) to a peak at about day 23 of pregnancy, then falls to undetectable levels at day 35, and remains undetectable throughout the rest of gestation. Serum estrone and estradiol levels rise and fall with RhCG titers in early pregnancy, reaching a nadir on day 35 of gestation before placental estrogen secretion (largely estradiol) supervenes. Circulating estrogens reach a high and variable plateau at about day 80 of pregnancy and rise to maxima on the day prior to parturition. Serum progesterone levels in early pregnancy, while rising abruptly at the outset of RhCG secretion, fall in the face of waxing RhCG titers and increase again only as RhCG levels fall. Ovariectomy on day 23 of pregnancy causes a sharp fall in circulating levels of estrogens and no compromise of the continuation of pregnancy. These data suggest that the order of hormone production by the placenta is RhCG. first discernable at about 10-I I days after ovulation, followed by progesterone, whose secretion by the placenta is initiated prior to day 23 of pregnancy since ovariectomy at this time causes no fall in circulating progesterone levels, and lastly, estradiol and estrone. which rise rapidly in peripheral serum after day 35 of pregnancy. These data support the hypothesis that the shortlived stimulation of progesterone secretion by the corpus luteum in early pregnancy is caused by the initiation of placental RhCG secretion and that the failure of Iuteal progesterone secretion to be maintained in the face of rising RhCG titers may be an expression of the luteolytic effect of the increased luteal estrogen production also stimulated by this gonadotropin.