Hormone-dependent subpopulation of rat testicular luteinizing hormone (LH) receptors.

Abstract

The effects of prolactin (PRL), growth hormone (GH), and luteinizing hormone (LU) treatment on testicular LI-I receptor content were studied in the hypophysectomized adult male rat. One and 2 weeks after hypophysectomy, testicular LH receptor binding capacity, as determined by 1125 1)hCG binding to whole testicular homogenates, was 14% and 16% of normal values, respectively. Seven days of s.c. LH treatment (5 pg/day), begun 1 week after hypophysectomy, caused a significant additional reduction of 1125 Il-hCG binding capacity to 10% of control values. Growth hormone administration (100 pg/day) for 7 days, begun 1 week after hypophysectomy, caused an increase in binding to 31% of control values, but simultaneous administration of LH (5 pg/day) prevented this GM-induced increase in binding capacity. Seven days of PRL treatment (100 pg/day) also caused a significant increase in [121 Il-hCG binding above the 2 week hypophysectomized control values (24%), but adding PRL to GH treatments did not result in an increase in 112511-hCG binding above that seen with GH or PRL alone. However, simultaneous administration of LH with PRL caused the induction of additional new receptors and returned total binding to 44% of normal intact control values. Combination of all three treatments (GH, PRL, and LH) showed an additive effect of the residual and PRL + LH treatment regimens and increased [12511 -hCG binding to 52% of that of normal controls. These experiments suggest 1) GM and PRL are capable of inducing new LII receptors in the regressed testis of the hypophysectomized rat, 2) PRL allows LH or LH allows PRL to induce a new LH receptor population resistant to LH down-regulation, 3) GIl causes the induction of a new population of LH receptors sensitive to LU down-regulation. These observations raise the possibility that subpopulations of Leydig cell LH receptors with different hormonal sensitivities reside within the testes.