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Acute subcutaneous (s.c.) administration of aldosterone increases ex vivo 22Na 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 beta-hydroxy-3-oxo,7 alpha-propyl(17 alpha)-pregn 4-ene, 21 potassium carboxylate] and spironolactone. The specific glucocorticoid receptor agonist RU 26988 [11 beta,17 beta-dihydroxy-17-(1-propynyl) androesta-1,4,6 trien-3-one] does not modify 22Na 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 22Na efflux and ouabain-independent 22Na efflux, which are completely blocked by actinomycin D; and 2) a very rapid increase of passive 22Na efflux, which is insensitive to actinomycin D and therefore does not seem to depend on transcription of genomic information.

Direct action of aldosterone on transmembrane 22Na efflux from arterial smooth muscle. Rapid and delayed effects.