The rescue of the primate corpus luteum (CL) by CG in early pregnancy is transient, despite a continued rise in circulating CG. To investigate the mechanisms resulting in this response, female rhesus monkeys were given im injections of increasing doses of hCG for 10 days during the menstrual cycle to mimic the pattern of circulating macaque CG observed in early pregnancy. Treatment began 5.3 ± 0.3 (early luteal phase; n = 4; mean ± se), 8.3 ± 0.5 (midluteal phase; n = 6), or 12.0 ± 0.4 (late luteal phase; n = 4) days after the midcycle LH surge. Femoral venous blood was collected daily from CG-treated animals from day 8 of the menstrual cycle until the onset of menses. Serum hCG, LH, progesterone (P), and 17β-estradiol (E) were measured by RIA. When CG treatment began during the early luteal phase, serum P increased within 9 h after the initial injection (P < 0.05); elevated concentrations of P persisted through treatment (range, 5.7-10.8 ng/ml) and decreased only after termination of CG injections. When treatment began during the midluteal phase, serum P increased within 9 h (P < 0.05), peaked the third day of CG treatment (10.4 ± 2.2 ng/ml), and then declined despite a continued rise in serum CG. Initiation of CG treatment late in the luteal phase also elicited a transient but less profound (peak, 6.4 ± 0.5 ng/ml) increase in P concentrations. Although P patterns differed among treatment groups (P < 0.01, by analysis of variance, split plot design), E patterns did not (P > 0.05). Serum E increased between 9 and 24 h after onset of treatment and remained elevated until 3-4 days after cessation of CG injections. In summary, treatment that elicited pregnancy-like increases in peripheral CG beginning in the midluteal phase of the menstrual cycle resulted in a transient stimulation of luteal P production similar to that observed in macaques during early pregnancy. This scheme provides a useful model for studying the primate CL during simulated early pregnancy. In contrast, CG administration begun early in the luteal phase resulted in persistent, rather than transient, stimulation of luteal P production. We conclude that the mechanisms involved in the transitory response of the primate CL to circulating CG during pregnancy are inoperative during the early luteal phase of the menstrual cycle.
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