Oral administration of 400μg of fludrocortisone acetate for three days suppresses aldosterone production in normal subjects with minimal effect on the excretion of Porter-Silber chromogens. Administration of fludrocortisone acetate to hypertensive patients with hyperaldosteronism suppressed aldosterone production into the normal range in all patients with essential hypertension and in one patient with adrenal nodular hyperplasia, but failed to do so in the patients with aldosterone-producing adenoma or nodular hyperplasia, confirmed subsequently. Administration of fludrocortisone acetate to hypertensive outpatients with hyperaldosteronism is an effective screening procedure for further evaluation of primary adrenal disease.