Long term spironolactone and the adrenal cortex in essential hypertension.
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.
D015070:18-Hydroxydesoxycorticosterone / Q000097:blood; D000302:Adrenal Cortex / Q000187:drug effects / Q000503:physiopathology*; D000328:Adult; D000368:Aged; D000450:Aldosterone / Q000097:blood / Q000652:urine; D003366:Cosyntropin; D005260:Female; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D006973:Hypertension / Q000188:drug therapy / Q000378:metabolism / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D013148:Spironolactone / Q000627:therapeutic use*
D015070:18-Hydroxydesoxycorticosterone; D003366:Cosyntropin; D013148:Spironolactone; D000450:Aldosterone; D006854:Hydrocortisone