Long term spironolactone and the adrenal cortex in essential hypertension

• Published in: Clinical endocrinology (Oxford) Vol. 13; no. 3; p. 273
• Main Authors: Lewis, P S, Gorchein, A, James, V H, May, C N, Horth, C E
• Format: Journal Article
• Language: English
• Published: England 01.09.1980
• Subjects: 18-Hydroxydesoxycorticosterone - blood; Adrenal Cortex - drug effects; Adrenal Cortex - physiopathology; Adult; Aged; Aldosterone - blood; Aldosterone - urine; Cosyntropin; Female; Humans; Hydrocortisone - blood; Hypertension - drug therapy; Hypertension - metabolism; Hypertension - physiopathology; Male; Middle Aged; Spironolactone - therapeutic use
• ISSN: 0300-0664
• DOI: 10.1111/j.1365-2265.1980.tb01054.x

In view of recent evidence that spironolactone may inhibit synthesis of corticosteroids by a direct effect on the adrenal cortex, adrenocortical function was studied in eight patients with essential hypertension who had been treated with spironolactone from 3 months to 14 years. Their 24 h renal excretion of adrenocorticoid metabolites and the responses of cortisol, aldosterone and 18-hydroxy-11 -deoxycorticosterone (18-OH-DOC) to an incremental infusion of tetracosactrin (1-24 ACTH) were compared with those in eight patients with recently diagnosed essential hypertension who had received no spironolactone. The spironolactone-treated group had a significantly higher excretion of aldosterone, whilst the excretion of other adrenocorticoid metabolites did not differ. The same group also required less tetracosactrin to stimulate a detectable rise of plasma cortisol and 18-OH-DOC, they had greater plasma 18-OH-DOC responses at all infusion rates and, at the lowest infusion rates, had greater aldosterone responses. These results indicate that long-term spironolactone therapy does not inhibit adrenocortical function and may have some stimulatory effects.