Mineralocorticoid Receptors, Salt, and Hypertension

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