Mineralocorticoid receptor (MR) antagonists have been used as potassium-sparing diuretics in hypertension. However, in addition to their diuretic and secondary blood pressure (BP)-lowering effects, there exists strong evidence from clinical and experimental studies that they prevent aldosterone-induced myocardial fibrosis independent of their effect on BP. Sustained elevation of aldosterone levels and increased sodium intake in animal models has been found to induce myocardial fibrosis. Fibrosis of the right ventricle, the atria, and the pulmonary artery supports the concept that these effects are BP independent, corroborated by the finding that spironolactone in a dosage not sufficient to lower BP prevents myocardial fibrosis. Patients suffering from primary hyperaldosteronism or Conn's adenoma show more myocardial fibrosis, as assessed by echocardiography, than essential hypertensive patients. Several mechanisms have been proposed to mediate the profibrotic effects of aldosterone, including the possibility of local aldosterone production in the heart, an increase of myocardial AT(1)-receptor density, and enhanced local angiotensin converting enzyme expression. Furthermore, aldosterone increases endothelin receptor expression, which also might cause myocardial fibrosis. Because of the pivotal importance of aldosterone binding to the MR, MR antagonists have emerged as attractive compounds that provide specific end organ protection beyond solely their antihypertensive effects.