Spontaneously hypertensive rats and rats made hypertensive by deoxycorticosterone-salt treatment have in common increased Na+ and K+ permeability and transport in their aortic cells. These changes may be important factors in the development of the hypertensive state and may be mediated by mineralocorticoid binding to intracellular sites in the aorta. Therefore, we examined 3H-aldosterone binding in aortic cell cultures from spontaneously hypertensive rats and normotensive Wistar-Kyoto rats. Vascular corticoid binding sites in the two strains were compared by Scatchard analysis of Kd and Bmax, pH and temperature stability, and subcellular binding. By all of these criteria normotensive rats. These results indicate that the underlying genetic defect in spontaneous hypertension is not an intrinsic cellular defect which alters mineralocorticoid binding in the aorta.