We evaluated a new method utilizing saralasin to differentiate primary aldosteronism due to an aldosterone-producing adenoma from idiopathic hyperaldosteronism. The test is based on the marked difference in sensitivity to angiotensin II of aldosterone-producing adenomas and hyperplastic adrenal glands and the partial angiotensin II agonist property of saralasin in low-renin states. Saralasin was infused into 14 patients with primary aldosteronism and the plasma aldosterone responses determined. Plasma aldosterone concentration increased in all eight patients with idiopathic hyperaldosteronism, whereas there was no increase in plasma aldosterone in six patients who had a solitary adenoma. We concluded that saralasin may be a clinically useful, noninvasive tool to distinguish patients with an aldosterone-producing adenoma from those who have idiopathic hyperaldosteronism.
Bibliographical noteFunding Information:
From the Section of Endocrinology, Metabolism, and Hypertension, Department of Medicine, University of Oklahoma College of Medicine, Oklahoma City, Okla. The Veterans Administration Hospital, Oklahoma City, Okla. and the Division of Endocrinology and Metabolism, Department of Medicine, Mayo Clinic and Mayo Foundation. Rochester, Minn, Supported in part by the Mayo Foundation, Norwich Pharmacal Co, USPHS General Clinical Research Grant RR-585. and Veterans Administration. Address reprint requests to Dr Ronald D. Brown, Department of Medicine, South Pavilion, PO Box 26307, Oklahoma City, OK 73126. 0 I984 by Grune & Straiton, Inc. 0026-0495/84/3308-0010$03.00/0