Attenuation of gonadotropin-releasing hormone reflex to coitus by alpha1-adrenergic receptor blockade in the rabbit.

The coitally induced gonadotropin-releasing hormone (GnRH)/luteinizing hormone (LH) surge in the rabbit is preceded by an enhanced secretion of hypothalamic norepinephrine (NE). To investigate if adrenergic receptors are essential for the GnRH/LH surge, we administered a specific alpha1 receptor blocker, prazosin, into either the arcuate nucleus-median eminence (AME) or the third cerebroventricle (3rd V) of tethered, freely moving intact female rabbits via push-pull perfusion (PPP). Dual cannulae for PPP and drug infusion were placed stereotaxically either into the AME or AME and 3rd V of each rabbit after insertion of a permanent femoral venous catheter for serial blood sampling. During an experiment, continuous PPP samples and 10-min intermittent blood samples were collected for 5-6 hr. Females received either prazosin or control medium (artificial cerebrospinal fluid into an AME or saline into a 3rd V cannula) for 4 hr, beginning 1 hr before coitus. Intraventricular infusion of prazosin significantly (P < 0.05) suppressed both the postcoital GnRH and the LH surges. Administration of prazosin into the AME also attenuated the magnitude of the postcoital GnRH surge (P < 0.05) whereas postcoital LH values were not decreased below that of the control group (P > 0.05). The results suggest that alpha1 receptors are physiologically active in the initiation of the postcoital GnRH release. These findings, along with our earlier report of enhanced postcoital NE secretion, reinforce the hypothesis that NE plays an essential role in the preovulatory GnRH/LH surge in rabbits.