Synchronous secretion of luteinizing hormone and prolactin in the human luteal phase: neuroendocrine mechanisms.

Studies of normal luteal phase women have shown that increases in serum LH and PRL are commonly synchronous. This study was designed to investigate the possible neuroendocrine mechanism(s) underlying this phenomenon. Six normal women were studied during the midluteal phase of 2 cycles. In the first cycle, they had blood samples collected at 15-min intervals for 6 h on 3 occasions during which time they received an infusion of normal saline or naloxone (1 mg/h) or a bolus of metoclopramide (10 mg, iv). In a second cycle, they received GnRH in increasing iv doses of 1, 10, and 50 micrograms at 2-h intervals. During the saline infusion, 11 of the 16 serum LH pulses (69%) were accompanied by an increase in serum PRL, and in 5 of the subjects, the first pulse of LH was synchronous with that of PRL (P = 0.0015). Naloxone increased the number of LH pulses from 16 to 20 and the number of PRL pulses from 12 to 16, all of which were synchronous with LH pulses. Administration of metoclopramide caused a substantial increase in PRL and a loss of further PRL pulsatility; however, LH pulsatility remained unaffected. Even after the smallest dose of GnRH (1 microgram), there was an increase in serum PRL [basal level, 11.8 +/- 2.1 (+/- SE) micrograms/liter; peak level, 16.5 +/- 3.3 micrograms/liter] as well as LH and FSH. The increase in serum PRL was, unlike the gonadotropin response, maximal after the 10-microgram dose of GnRH (peak level, 23.2 +/- 6 micrograms/liter) and did not increase further after the 50-micrograms dose (peak level, 18.5 +/- 2.4 micrograms/liter). These studies demonstrate that there is a PRL response to GnRH in the luteal phase and suggest that the observed synchrony in LH and PRL secretion at this time results from a physiological response of both the gonadotrope and the lactotrope to endogenous GnRH.