Mineralocorticoid antagonism and cardiac hypertrophy.

Aldosterone provides circulatory support by promoting reabsorption of sodium in exchange for potassium in the kidney. Mineralocorticoid receptors (MRs) are found in nonepithelial (vessel, heart, and brain) and epithelial tissues. Excess aldosterone may exert harmful effects by provoking hypertrophy and fibrosis in the cardiovascular system, thus contributing to reduced vascular compliance and increased ventricular stiffness. Primary aldosteronism is the most common cause of mineralocorticoid-induced hypertension, and MR antagonism offers the best prospect for achieving therapeutic goals. MR blockade also ameliorates pathological changes in the heart in the setting of low-aldosterone hypertension. The beneficial cardiac effects of MR antagonists are likely attributable, at least in part, to attenuation of myocardial oxidative stress and coronary vascular inflammation induced by activation of MRs. MR antagonism thus may have wide therapeutic potential in various cardiovascular diseases, with its benefit not limited to those characterized by aldosterone or salt excess.