Studies on the Mechanism of the Suppression of the Preovulatory Surge of Luteinizing Hormone in the Rat by Arginine Vasotocin

Abstract

The finding that iv injections of 8- arginine vasotocin (AVT) inhibit the preovulatory surge of luteinizing hormone (LH) in the proestrous rat prompted studies to characterize the physiological mechanisms involved in this process further. Intraventricular injections of AVT (0.2 μg every hour from 1300 to 1600 h) in proestrous rats eliminated the preovulatory LH surges in 75% of the animals and the remaining 25% showed delayed surges. Similar AVT administration at the 0.0001 μg level resulted in complete elimination of the surge in approximately 33% and a delayed surge in 50%. In additional studies, steroid-primed rats 14 days after ovariectomy received 15 μg prostaglandin E2 (PGE2) in 5 μl of diluent intraventricularly, producing approximately a 4-fold increase in LH within 10 min. Administration of AVT both iv (doses of 0.5, 1.0, and 2.0 μg) and intraventricularly (0.1 μg) every 30 min for 90 min before PGE2 injection had no eifect on the LH rise. Electrochemical stimulation with 1000 μA for 30 sec in the medial preoptic area of proestrous rats at a time near the critical period produced approximately a 3-fold increase of LH within 1 h. Intravenous doses of 0.5, 1.0, and 2.0 μg AVT every 30 min for 3 h, commencing 2 h before stimulation, did not affect the LH rise. We conclude that AVT acts to inhibit the endogenous LH surge at a higher neuronal level than the PGE2-induced release of LH-releasing hormone (LHRH), although not between the medial preoptic area and the LHRH neurons. Furthermore, the data indicate that picogram amounts of AVT, acting via the central nervous system, selectively suppress the cyclic release of pituitary LH, thereby regulating fertility through inhibition of ovulation.