Aldosterone secretion and primary and malignant hypertension.

After the synthesis of desoxycorticosterone (DOC), it became apparent that this corticosteroid, the physiological effects of which are concerned primarily with sodium and potassium metabolism, can produce a state of hypertension both in animals and in man (1, 2). The induced hypertension is dependent upon the administration of adequate amounts of dietary sodium, whereas the hypertensive state, produced by administration of glucocorticoids such as cortisone, differs in that it is independent of the dietary sodium content (3). More recently, following the chemical and biological characterization of the mineralocorticoid hormone, aldosterone (4), a disease state associated with primary hypersecretion of this hormone has been described in man (5). Aldosterone produces effects on sodium and potassium metabolism similar to those of desoxycorticosterone, and the clinical syndrome of primary aldosteronism resembles the disease state produced by chronic administration of DOC to dogs (6). Arterial hypertension has been a consistent finding in patients with primary hyperaldosteronism. A number of other observations have suggested a relationship between the dietary sodium intake and the blood pressure level of patients with primary (benign essential) hypertension. The beneficial effects of sodium deprivation, and of various natriuretic agents in certain patients with hypertension, is well known. In addition, other studies have suggested that abnormalities of intracellular sodium and potassium content may occur in patients with arterial hypertension (7). Genest, Koiw, Nowaczynski and Lebouef (8) have re-