The Dahl salt-resistant substrain of Sprague-Dawley rats represents a uniform population of animals that are resistant to salt and mineralocorticoid induced hypertension. Aldosterone binding in the aortae of these rats is contrasted to that of age- and sex-matched rats of the Dahl salt-susceptible strain in an effort to identify a mechanism for resistance to salt induced hypertension. Cultured smooth muscle cells of both substrains contain two classes of aldosterone binding sites: corticoid receptor I with high affinity and low capacity, and corticoid receptor II with low affinity and high capacity. No differences were found between the two substrains in the affinities or binding capacities of these receptors. Both groups of Sprague-Dawley rats had a significantly higher corticoid receptor I affinity than the salt resistant Fischer 344 rats, a strain with a two-fold lower affinity than salt sensitive strains. These results indicate that an intrinsic defect in mineralocorticoid binding in aortic smooth muscle cells could not account for the resistance to salt and mineralocorticoid induced hypertension seen in Sprague-Dawley rats and that the biochemical abnormality underlying salt resistance is likely to be different from that of Fischer 344 rats.