Abstract

Previously, aldosterone has been shown to be a predominant or complete agonist in glucocorticoid effector systems, and to have a moderately high affinity for glucocorticoid receptors. Recently, in two mouse tissues (AtT-20 pituitary cells, liver cytosol) Miras and Harrison reported aldosterone to be without affinity for [ 3H]-triamcinolone binding sites [1]. In view of the possible implications for glucocorticoid receptor ontogeny, and mineralocorticoid specificity, we have repeated these studies on mouse liver, and extended them to kidney. In our hands, aldosterone has a moderately high affinity for glucocorticoid receptors in mouse liver and kidney, indistinguishable from that found in parallel studies in the rat.

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