Abstract

Screening tests for primary aldosteronism were compared in 22 patients with this disorder and 140 hypertensive controls. Adequate (93-100%) sensitivity and specificity were not provided by single tests ((1) serum K, (2) furosemide-stimulated PRA, or (3) plasma aldosterone concentration (PAC) after furosemide, or (4) after 2 liters 0.9% NaCl)), but were provided by combinations: (2) + (1) or (3); (2) + (1) or (4); and by a pressor response to saralasin + (3) or (4). Mechanism of the observed excessive rise in PAC "stimulated" by furosemide and standing for 2 h was studied in the same patients. The rise in "stimulated" PAC was (a) associated with a low PRA and not reproducible by angiotensin II infusions; (b) associated with a slight but significant rise in plasma cortisol and was reproducible by ACTH infusions. It is, therefore, attributed to the effects of slight ACTH release acting on adrenal tissue with super-sensitivity of aldosterone response to ACTH.

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