Anterior pituitary hormonal regulation of testicular gonadotropin-releasing hormone receptors.

Testicular GnRH receptors are increased 2-fold 1 day after hypophysectomy and remain elevated for up to 6 days. Consequently, the present study was undertaken to determine which pituitary hormone(s) regulated testicular GnRH receptors. Adult male rats were hypophysectomized and injected sc every 8 h for 2 days with LH, FSH, GH, PRL, estradiol, testosterone, 5 alpha-dihydrotestosterone, and vehicle (controls), beginning within 5 h of surgery. The animals were decapitated on the third day after hypophysectomy, the testes were excised, and interstitial tissue was teased from seminiferous tubules before storage at -70 C until assayed. The analog D-Ala6-des-Gly10-GnRH ethylamide was used to assess GnRH receptors on 10,800 X g-membrane fractions of interstitial tissue. The administration of GH, PRL, and FSH at concentrations which maintained LH receptors in adult or immature hypophysectomized rats did not prevent the increase in GnRH receptors, whereas LH replacement prevented the rise in GnRH analog binding in a dose related manner. LH also reduced preexisting posthypophysectomy increases in GnRH receptor concentrations. Injections of estradiol (5 micrograms/day) partially inhibited the posthypophysectomy increase in GnRH receptors, whereas the androgens 5 alpha-dihydrotestosterone and testosterone were ineffective. These results indicate that LH can regulate testicular GnRH receptors. Since GnRH directly inhibits testosterone secretion, inhibition of testicular GnRH receptors by LH may be one of the mechanisms by which LH replacement enhances testosterone production after hypophysectomy.