Abstract
The effects of corticotropin (ACTH) on adrenocortical steroidogenesis were studied on rabbit adrenocortical cells harvested from control animals and from ACTH-treated rabbits. Treatment (200 μg ACTH 1–24 s.c. daily for 12 days) led to an increase in the maximal secretory capacity of a given number of adrenocortical cells in response to ACTH as well as to dibutyryl c-AMP in vitro. This increase in the steroidogenic activity of ACTH was associated with a clearcut reduction in the sensitivity to the peptide, as much higher concentrations of ACTH were needed to elicit a half-maximal increase in steroidogenesis with cells from ACTH-treated animals. Moreover, the ACTH-dependent generation of c-AMP was significantly reduced as a result of in vivo treatment with ACTH. The production of aldosterone in response to ACTH or dibutyryl c-AMP was also much lower with cells from ACTH-treated rabbits. In addition to quantitative changes in steroidogenesis, prolonged treatment with ACTH led to increased generation of 17-hydroxylated steroids, with increased adrenocortical production and plasma levels of cortisol. cortisone and 11-deoxycortisol; concomitantly synthesis and circulating levels of corticosterone were reduced. It was therefore concluded that besides the well-known prolonged trophic influence of ACTH on adrenal growth this peptide influences in a lasting way the function of adrenocortical cells. The latter effect is characterized in the rabbit by an increased capacity but decreased sensitivity to ACTH, and by a stimulation of 17α-hydroxylase activity with ensuing shift from corticosterone to cortisol production.
Published Version
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