Direct Action of Aldosterone on Transmembrane Na Efflux from Arterial Smooth Muscle Rapid and Delayed Effects

Acute subcutaneous (s.c.) administration of aldosterone increases ex vivo "Na 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 [17/3hydroxy-3-oxo,7 a-propyl(17 a)-pregn 4-ene, 21 potassium carboxylate] and spironolactone. The specific glucocorticoid receptor agonist RU 26988 [ll/3,17/3-dihydroxy-17-(lpropynyl) androesta1,4,6 trien-3-one] does not modify Na 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-dependent Na efflux and ouabaln-independent Na efflux, which are completely blocked by actinomycin D; and 2) a very rapid increase of passive Na efflux, which is insensitive to actinomycin D and therefore does not seem to depend on transcription of genomk information. (Hypertension 6: 425-430, 1984)