Clinical Pharmacology
ACTH stimulates the adrenal cortex to secrete cortisol, corticosterone, aldosterone, and a number of weakly androgenic substances. Although ACTH does stimulate secretion of aldosterone, the rate is relatively independent. Prolonged administration of large doses of ACTH induces hyperplasia and hypertrophy of the adrenal cortex and continuous high output of cortisol, corticosterone and weak androgens. The release of ACTH is under the influence of the nervous system via the corticotropin regulatory hormone released from the hypothalamus and by a negative corticosteroid feedback mechanism. Elevated plasma cortisol suppresses ACTH release.
The trophic effects of ACTH on the adrenal cortex are not understood beyond the fact that they appear to be mediated by cyclic AMP.
ACTH rapidly disappears from the circulation following its intravenous administration; in man the plasma half-life is about 15 minutes.
The maximal effects of a trophic hormone on a target organ are achieved when optimal amounts of hormone are acting continuously. Thus, a fixed dose of ACTH will demonstrate a linear increase in adrenocortical secretion with increasing duration for the infusion.