Aldosterone--villain or bystander?

Abstract

The two primary regulators of aldosterone secretion are potassium and the renin–angiotensin system. The latter is involved in volume homeostasis, with high salt intake suppressing the renin–angiotensin system and aldosterone levels and low salt intake having the opposite effect. Secondary hyperaldosteronism, a physiologic response to dietary salt restriction, promotes renal sodium conservation. In this setting, hyperaldosteronism is a bystander that has no cardiovascular consequences. Hyperaldosteronism emerges as villain in persons whose dietary salt intake is normal if the production of aldosterone is inappropriate for the level of sodium intake, resulting in excessive renal sodium retention, potassium wasting, hypertension, and cardiovascular . . .