Regulation of Leydig Cell Function by Prolactin, Growth Hormone and Luteinizing Hormone

The effects of prolactin (PRL), growth hormone (GH) and luteinizing hormone (LH) on testicular LH receptor concentration and on testosterone synthesis in response to LH (testicular responsiveness) was studied in mature intact and hypophysectomized rats. Hypophysectomy reduced LH receptor concentration by 80 o/o and testicular responsiveness to LH by 70a/o , 7 days after surgery. Daily treatment with LH initiated immediately following surgery resulted in a further dose-dependent decrease in LH receptors and a dose-dependent increase in testicular responsiveness. Loss of LH receptors was not due to occupancy of the receptor by exogenous LH. PRL (150 pgiday) or GH (150 pgiday) partially prevented the loss of LH receptors in hypophysectomized saline-treated rats. The effect of PRL plus GH on LH receptor concentration was additive. The combination of LH (5 ,pg/day), PRL and GH prevented any loss of LH receptors after hypophysectomy. A positive effect of LH on its receptor occurred in the presence of PRL. Treatment of hypophysectomized rats with 5 p g L H + 150 pg PRL enhanced the effect observed with PRL alone on maintenance of LH receptors. PRL, administered together with higher doses of LH (25 or 50 pgiday) prevented LH from exerting a negative effect on LH receptor concentration. Similar treatment with GH plus LH neither allowed a positive effect of LH nor prevented higher doses of LH from exerting a negative effect on LH receptor concentration. Loss in testicular LH receptors was also demonstrated in intact rats which received a single administration of LH. Administration of 150 p g PRL for 3 days partially prevented the LH-induced loss in LH receptors, while treatment with 150 p g GH had no effect on LH-induced loss of testicular LH receptors. Despite the ability of PRL to increase LH receptor concentration in hypophysectomized rats, PRL treatments did not enhance testicular respon-