Acute subcutaneous (s.c.) administration of aldosterone increases ex vivo22Na efflux from rat tail artery smooth muscle, which appears to be due to a specific action on mineralocorticoid receptors. Indeed, this effect is blocked by the antimineralocorticoid compounds RU 28318 [17ß- hydroxy-3-oxo,7 α-propyl(17 α)-pregn 4-ene, 21 potassium carboxylate] and spironolactone. The specific glucocorticoid receptor agonist RU 26988 [11ß,17ß-dihydroxy-17-(l- propynyl) androesta- 1,4,6 trien-3-one] does not modify22Na efflux. We show here that aldosterone has, at physiological concentrations, a mineralocorticoid specific stimulating effect on passive and sodium pump dependent transmembrane movements of sodium from the rat tail artery smooth muscle. Aldosterone exerts two types of action on sodium transport: 1) a delayed stimulation of ouabain-dependent22Na efflux and ouabaln-independent22Na efflux, which are completely blocked by actinomycin D; and 2) a very rapid increase of passive22Na efflux, which is insensitive to actinomycin D and therefore does not seem to depend on transcription of genomk information.