The classic effects of aldosterone on electrolyte transport are well defined. Recent studies have also identified effects of aldosterone on vascular resistance, on the central regulation of blood pressure, and on the pathogenesis of cardiac fibrosis. Our understanding of the mechanisms of aldosterone action has been enhanced by further studies of the mineralocorticoid receptor, by the identification of "nongenomic" actions, and by studies of the epithelial sodium channel (ENaC) genes. The ENaC subunit genes are mutated in conditions of both apparent mineralocorticoid deficiency (pseudohypoaldosteronism) and excess (Liddle's syndrome). These findings demonstrate the central role of these channels in the aldosterone-sensitive epithelial sodium transport pathway. ENaC subunit expression and another recently identified gene, the channel-inducing factor gene, or CHIF, are regulated by aldosterone in the rat distal colon. It remains to be determined whether this regulation represents a primary response to aldosterone.
|Number of pages||7|
|Journal||Current Opinion in Endocrinology & Diabetes|
|Publication status||Published - 1997|