Abstract Hypersecretion of 18-hydroxydeoxycorticosterone (18-OHDOC) may be implicated in some cases of low renin hypertension and in salt-sensitive hypertension in Dahl rats. To investigate the mechanism of action of the steroid, the binding of tritiated 18-OHDOC was studied in cytoplasmic fractions of kidney, liver and heart. Binding was displaceable by excess unlabelled 18-OHDOC, but to sites with affinity too low for a physiological role as 18-OHDOC receptors. Similarly, no specific high affinity plasma binding protein could be demonstrated ; by equilibrium dialysis, high capacity albumin binding was shown to be ~65%. The weak mineralocorticoid effects of 18-OHDOC would therefore appear to be mediated by occupation of physiological aldosterone receptors, and not by occupation of physiological receptors specific for 18-OHDOC itself.