Mineralocorticoid Response to Low Dose Adrenocorticotropin Infusion*

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Abstract
The adrenocorticoid responses to low dose ACTH of plasma aldosterone (aldo), corticosterone (B), 11-deox-ycorticosterone (DOC), 18-hydroxycorticosterone (18-OHB), 18-hydroxydeoxycorticosterone (18-0H-D0C), and cortisol (F) were compared. αACTH (l–24) was infused beginning at 0800 h at increasing rates from 12.5–200 mIU⁄30 min in supine normal subjects under the following conditions: 1) regular Na (120 meq) diet, 2) lowNa (10 meq) diet, 3) dexamethasone preadministra-tion (0.5 mg every 6 h for 48 h), and 4)night study (2000 h; 120-meq Na intake). Plasma 18-OH-DOC and B demonstrated quantitatively the greatest responses to ACTH, while DOC and 18-OHB responses were intermediate. Increments in aldo and F were least after ACTH and were maximum at 50 mIU⁄30 min ACTH, whereas other corticosteroids demonstrated linear responses up to infusionrates of 200 mIU⁄30 min. All corticoste-roids, however, were similar in their threshold responses to ACTH which were at infusion rates of approximately 7–9 mlU⁄ 30min. Na restriction enhanced aldo and 18-OHB responses to ACTH 2- to 3-fold but did not alter the other corticosteroid responses. Dexamethasone pretreatment augmented aldo, 18-OHB, and F responses but did not change the responsivity of the other corticosteroids to ACTH. Adrenal corticosteroid responses to ACTH were not significantly different between 0800 and 2000 h in subjects on 120-meq Na intake. Thus, corticoste-roids show markedly different responses to physiological doses of ACTH, which may have more importance in their regulation than heretofore proposed. Dexamethasone pretreatment enhances aldo, 18-OHB, and F responses to ACTH but does notaffect the responses of other corticosteroids. Contrary to reports in experimental animals, corticosteroid responses to ACTH in man do not differ from day to night.

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