Effects of Aldosterone and Cortisol on Human Erythrocyte Na Efflux

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Abstract
Sodium efflux rate constants from erythrocyte ghosts or intact red blood cells were measured in 5 patients with primary hyperaldosteronism, 2 patients with secondary hyperaldosteronism, and 3 patients with Cushing's syndrome. In all of them but one patient with primary hyperaldosteronism, a marked increase in active outward Na transport was demonstrated in erythrocyte ghosts and confirmed in all 6 patients whose intact red blood cells were studied as well. Erythrocyte intracellular Na concentrations were low in the patients with Cushing's syndrome and normal in the hyperaldosteronism patients. Both groups of patients had elevated erythrocyte Na+K dependent ATPase activity. Measurements of Na efflux rate constants in 3 patients after bilateral adrenalectomy revealed normal values. The in vitro incorporation of aldosterone 10−6.7m or cortisol 10−5.6m in erythrocyte ghosts from control subjects produced significant increases in active Na efflux rate constants. This effect was abolished by simultaneous incorporation of equimolar amounts of spironolactone. Cortisone, 11-deoxycortisol and various reduced corticosteroids were without effect in this system. Spironolactone 10−5m or 10−6m had no significant effect by itself, but 10−4m inhibited active transport in ghosts from control subjects and from 1 patient with hyperaldosteronism. None of the agents studied had any effect on the intact cell system in vitro. The mechanism of action of cortisol and aldosterone on Na flux across red blood cell membranes must be different from the mechanism currently postulated for their action on toad bladder cells since mature erythrocytes have no nuclei and are not known to produce new protein.

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