Examination of Prolactin and Pituitary-Adrenal Axis Components as Intervening Variables in the Adrenalectomy-Induced Inhibition of Gonadotropin Response to Castration*

Publisher Website
Google Scholar
Abstract
Adrenalectomy performed at the same time as or 12 h after castration delays the postcastration rise in LH [luteinizing hormone] and FSH for at least 12 h. Three mechanisms previously advanced as possible mediators in this suppression were tested. Blocking PRL [prolactin] 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. 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. 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. The adrenalectomy-induced suppression of LH could be due to a neurally mediated stress response probably resulting in suppression of GnRH secretion. In other treatment groups, cortisol was implanted 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 animals, and restored castration-adrenalectomy. This divergence between LH and FSH secretion suggests that the effect of adrenalectomy on the 2 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. LH and FSH apparently are regulated by different mechanisms under many experimental conditions, including stress and elevated corticoid levels.