Induction of Relaxin Secretion in Rhesus Monkeys by Human Chorionic Gonadotropin: Dependence on the Age of the Corpus Luteum of the Menstrual Cycle 1

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Abstract
Peripheral concentrations of immunoreactive relaxin are undetectable in primates during the nonfertile menstrual cycle, but become measurable during the interval when chorionic gonadotropin (CG) rises in early pregnancy. Whether exogenous CG, administered in a dosage regimen which invoked patterns and concentrations resembling those of early pregnancy, would induce relaxin secretion in nonpregnant rhesus monkeys, and whether the induction was dependent on the age of the corpus luteum (CL) at the onset of treatment was investigated. Female rhesus monkeys received twice-daily i.m. injections of increasing doses of human CG (hCG) for 10 days beginning in the early (n = 4), mid (n = 6) or late (n = 4) luteal phase of the menstrual cycle [5.3 .+-. 0.3, 8.3 .+-. 0.5, and 12.0 .+-. 0.4 days after the midcycle luteinizing hormone (LH) surge, respectively; .hivin.x .+-. SEM [standard error of the mean]]. Whereas immunoreactive relaxin was nondetectable in the luteal phase of posttreatment cycles, detectable levels of relaxin were observed in 2 of 4, 5 of 6, and 3 of 4 monkeys during hCG treatment in the early, mid and late luteal phase, respectively. Although CG treatment rapidly enhanced progesterone levels, the appearance of relaxin was deferred; relaxin was first detectable 9.0 .+-. 1.0 and 4.7 .+-. 1.9 days after the onset of CG treatment at early and late luteal phases. Patterns of relaxin concentrations differed among groups (P < 0.05, ANOVA; split plot design) and relaxin levels were lowest (P < 0.01) in monkeys treated during the early luteal phase. Relaxin secretion typically began as progesterone declined and peak levels of relaxin were achieved in 9 of 10 monkeys after progesterone levels dropped to < 2 ng/ml. Induction of relaxin secretion by CG was a function of the age of the CL of the menstrual cycle. Notably, the mechanisms which promote relaxin secretion did not appear to be fully operational in the young, developing CL. Peak relaxin secretion in the rhesus monkey was associated with declining steroidogenic function of the CL. Initiation of the hCG regimen in nonpregnant monkeys at the expected time of implantation provides a model for studying the mechanisms regulating relaxin, as well as steroid, secretion by the macaque CL of early pregnancy.