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It is well known that aldosterone, by its effects on renal tubular reabsorption of sodium, plays an important role in reducing renal excretion of sodium, both in response to sodium deprivation and in pathological states of fluid retention (2). Excessive aldosterone output has been shown to be associated with reduced sodium concentrations in sweat and saliva (3). It is probable that this mineralocorticoid, like desoxycorticosterone acetate (DCA) (4), reduces the sodium content of the feces (5). Woodbury and Koch (6) have shown that aldosterone significantly decreases the intracellular sodium concentration in the brain and skeletal muscle of mice. It is unlikely that these actions of the hormone on different cells and tissues in the body are entirely secondary to the action on the renal tubule. Indeed, aldosterone has been shown to influence sodium transport in toad bladder in vitro (7) and to have a direct stimulatory effect on the contractility of smooth muscle (8) and myocardium (9). This evidence that the steroid acts directly on a variety of different tissues led us to study its action on sodium transport between the plasma and the cells of the blood. Previously unsuccessful attempts to demonstrate an effect of aldosterone on erythrocytes (10-12) might have resulted from technical difficulties in measuring sodium exchange, both because human erythrocytes contain only small amounts of sodium that exchange very slowly (13) and because the blood used presum-

Retardation of Sodium Exchange in Dog Erythrocytes by Physiological Concentrations of Aldosterone, in Vitro*