The role of LH in regulation of Leydig cell responsiveness to an LHRH agonist.

The short-term relationship between deprivation of LH and changes in the responsiveness of isolated Leydig cells to an LHRH agonist was studied in adult rats injected with a potent antiserum to oLH. This treatment suppressed serum and intra-testicular levels of testosterone within 4 h of injection by 80-90% and 70%, respectively, with further suppression to levels found in hypophysectomized rats by 20 h. At 12-20 h after antiserum injection there was no major consistent change from control values in the number of Leydig cell LH (hCG)-receptors or in the testosterone response of the cells to hCG-stimulation. In the same cells the number of LHRH-receptors and the maximal testosterone response to LHRH agonist were increased (P less than 0.001) by 50% or more, although the magnitude of increase varied considerably between experiments. The ability of LHRH agonist to enhance the testosterone response of cells to hCG-stimulation was also increased significantly (P less than 0.001) in antiserum-treated rats. Comparable changes in testosterone responsiveness to LHRH agonist were observed following purification of Leydig cells on Percoll gradients. Although there was some evidence for changes in Leydig cell LHRH-receptor numbers and responsiveness to LHRH agonist at 4 h after intravenous antiserum injection, these changes were small compared with changes seen at later times. It is concluded that Leydig cell responsiveness to an LHRH agonist is negatively regulated by LH, and this has implications with respect to a possible role of 'testicular LHRH' in regulation of the intra-testicular levels of testosterone.