Mineralocorticoid Receptors, Salt, and Hypertension

This review, covering work from the Baker Institute and elsewhere, is divided into four sections. In the first a summary account of two areas - mineralocorticoid receptors and the enzyme 11β hydroxysteroid dehydrogenase - will be given as background. Next is a brief consideration of the three single-gene causes of human hypertension described to date - glucocorticoid-remediable aldosteronism, Liddle's syndrome, and apparent mineralocorticoid excess - in all of which abnormal sodium handling is a feature. Third, the sequelae of aldosterone occupancy of nonepithelial mineralocorticoid receptors will be analyzed in some detail by reviewing studies on experimental mineralocorticoid hypertension and cardiac fibrosis from this laboratory and elsewhere. Finally, three recent studies from this laboratory will be presented: on putative 11-ketosteroid receptors in epithelial tissue, on glucose-PKC potentiation of mineralocorticoid effects on heart cells, and on the necessity for factors/ processes other than the conversion of cortisol to cortisone (or, in the rat, corticosterone to 11-dehydrocorticosterone) to ensure aldosterone-specific effects in mineralocorticoid target tissues.