Abstract
The effects of prolonged treatment with corticotropin (ACTH 1–24, 200μg s.c. daily during 12 days) on the production of androgens and glucocorticoids were studied on rabbit dispersed adrenocortical cells. The steroidogenic capacity of adrenocortical cells, expressed in terms of the maximal response to ACTH of glucocorticoid (i.e. corticosterone and cortisol) production, was significantly increased after treatment with ACTH. This was associated with a loss of sensitivity to this peptide: indeed, the concentration of ACTH required to induce a half maximal secretory response was one order of magnitude higher with cells from ACTH-treated animals. Among the C 21 steroids measured the changes observed involved the 17α-hydroxylated compounds (cortisol, cortisone, 11-deoxycortisol) while corticosterone production was significantly depressed. This effect of prolonged ACTH treatment on steroidogenic pathways involving 17α-hydroxylation, was further evidenced by a clear-cut enhancement in androgen secretion (dehydroepiandrosterone, androstenedione and testosterone) by adrenocortical cells from ACTH-treated animals. The changes observed after treatment of the animal with ACTH were equally obvious, whether the adrenocortical cells were incubated with ACTH or with dibutyryl-c-AMP.
Published Version
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