Stimulation and suppression of aldosterone in plasma of normal man and in primary aldosteronism

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Abstract
The effect of stimulating and suppressive influences on plasma aldosterone in normal man and in patients with primary aldosteronism were studied using a sensitive double-isotope derivative assay for aldosterone. In normal sitting subjects, values were 9.2±0.9 (SE) mμg/100 ml and in subjects supine for 1 hr plasma aldosterone was 5.2±0.4 (SE) mμg/100 ml. Adrenocorticotropic hormone (ACTH), 0.5 U/hr, produced a rise of 46.8±22 (SE) mμg which was similar to the 1-hr effect of an infusion of a synthetic ACTH (β1-24, Cortrosyn). Angiotensin II in pressor amounts also increased plasma aldosterone 21.5±2.9 (SE) without change in plasma cortisol, whereas a subpressor dose ([unk]) had minimal effect. Fludrocortisone, 1.2 mg/day for 3 days, suppressed plasma aldosterone levels to 1.8±0.7 (SE) mμg/100 ml in five normal sitting subjects (P < 0.01); however, dexamethasone, 2 mg/day for 1-2 days, did not lower aldosterone concentration in plasma. In six patients with primary aldosteronism, plasma aldosterone on a normal sodium diet was 39.1±4.4 (SE) which differed significantly from normal sitting or supine subjects (P < 0.001). In contrast to the normal subjects, neither a pressor infusion of angiotensin II for 1 hr, nor fludrocortisone, 1.2 mg/day for 3 days, impressively altered plasma aldosterone levels. This approach appears to be useful for the study of the acute physiology and control mechanisms of aldosterone production in normal and hypertensive man.