Examination of prolactin and pituitary-adrenal axis components as intervening variables in the adrenalectomy-induced inhibition of gonadotropin response to castration.

Abstract

Adrenalectomy performed at the same time as, or 12 h after, castration delays the postcastration rise in LH and FSH for at least 12 h. We tested three mechanisms previously advanced as possible mediators in this suppression: 1) blocking PRL in castrate-adrenalectomized males with bromoergocryptine did not restore the normal postcastration rise in serum LH and FSH, eliminating high PRL levels as a cause of this gonadotropin suppression; 2) exogenous ACTH given at the time of orchidectomy did not inhibit either gonadotropin, eliminating high peripheral ACTH as an agent of adrenalectomy-induced suppression of LH and FSH; and 3) intestinal traction performed at the same time as orchidectomy suppressed the secretion of LH and FSH to the same degree as adrenalectomy, ruling out the lack of any adrenal factor as a means by which adrenalectomy blocked gonadotropin secretion. Our data suggest that the adrenalectomy-induced suppression of LH is due to a neurally mediated stress response probably resulting in suppression of GnRH secretion. In other treatment groups, we implanted cortisol before surgery to test the effect of ACTH suppression on LH and FSH secretion in castrate-adrenalectomized animals. A striking divergence between LH and FSH was seen in response to cortisol treatment. Cortisol suppressed LH, but not FSH, in castrate animals, and restored postcastration FSH, but not LH, secretion 12 h after combined castration-adrenalectomy. This divergence between LH and FSH secretion suggests that the effect of adrenalectomy on the two gonadotropins might result from different mechanisms. It is also possible that the differential effect of cortisol on LH and FSH secretion is not relevant to the effect of adrenalectomy on the postcastration secretion of these gonadotropins. These data add to the evidence, however, that LH and FSH are regulated by different mechanisms under many experimental conditions, including stress and elevated corticoid levels.