The purpose of this study was to examine the effect of a single injection of ACTH-(1-39) on gonadotropin secretion in the estrogen-primed intact and ovariectomized female rat and to determine if the effect of ACTH was mediated through the release of adrenal steroids. Administration of 100 μg ACTH-(1-39)/rat caused a significant elevation in serum LH and FSH levels 6 h after injection. This stimulatory action of ACTH was abolished by adrenalectomy in both intact and ovariectomized rats, suggesting that the effect was mediated through the adrenal. A requirement for estrogen priming was demonstrated by a lack of ACTH effect in nonestrogen-primed intact rats. The specificity of ACTH-(1-39) was demonstrated by the absence of effect on FSH and LH secretion by αMSH and ACTH-(4-10). Fifteen and 30 min after ACTH stimulation, the adrenal secreted significantly elevated amounts of both progesterone and corticosterone. RU486, which has both antiglucocorticoid and antiprogestin activity, effectively blocked the action of ACTH on gonadotropin secretion. Of the two steroids secreted by the adrenal after ACTH administration, progesterone, but not corticosterone, was able to induce a gonadotropin surge. Since estrogen priming is important for progesterone receptor development, the stimulatory action of ACTH appears to be mediated through progesterone acting through the progesterone receptor. These studies demonstrate that ACTH treatment in the estrogen-primed rat can stimulate LH and FSH secretion through adrenal progesterone secretion.
ASJC Scopus subject areas