Blockade of rat testicular gonadotropin releasing hormone (GnRH) receptors by infusion of a GnRH antagonist has no major effects on Leydig cell function in vivo

Abstract

The purpose of this study was to examine the physiological functions of the gonadotropin releasing hormone (GnRH) receptors present in the rat testis. The receptors were blocked in situ by infusing one testis of adult rats for 7 days with 10–100 ng/h of a potent GnRH antagonist (N-Ac-Ala1, d-p-Cl-Phe2, d-Trp3,6-GnRH) using Alzet osmotic minipumps. The contents of the pump were delivered to the testis through a cannula perforating, and fixed, to the tunica albuginea. A plastic cannula alone was attached to the contralateral testis, to act as a control. Infusion of the antagonist resulted in a dose-dependent decrease of testicular GnRH receptors, up to 90%. Some of the antagonist also occupied GnRH receptors in the contralateral testis and pituitary, but these effects were always clearly less than in the infused testis. None of the doses used affected circulating levels of gonadotropins, prolactin (Prl) or testosterone. However, when the endocrine parameters of the two testes were compared, the 100 ng/h dose of the antagonist resulted in a significant (P < 0.01−0.05) 16–32% decrease in the testicular content of testosterone, and LH, FSH and lactogen receptors. Similar effects (inhibition of the same parameters by 22–42%) were observed when immature (30-day-old) male rats were treated for 1 week with intratesticular infusions of the antagonist. It is inferred from these observations that, in physiological circumstances, testicular GnRH receptors may mediate stimulatory effects of Leydig cell LH and lactogen receptors, and testosterone synthesis. The changes observed were only subtle, which implies that the paracrine regulation through binding of a putative endogenous GnRH-like substance to testicular GnRH receptors plays a limited role in modulating Leydig cell activity.