A relatively selective competitive mineralocorticoid (aldosterone) receptor antagonist. Binds selectively to mineralocorticoid receptors and has low (less than 1%) affinity for glucocorticoid, progesterone, and androgen receptors. It is a competitive antagonist of aldosterone at mineralocorticoid receptors in the kidney, myocardium, salivary gland, GI tract, brain, and vasculature, and has been shown to inhibit the physiologic effects of aldosterone in these organs. Some of the antihypertensive effects of eplerenone may be related to restoration of endothelial function by increasing the release of nitric oxide, which results in vasodilation. Has been shown to produce sustained increases in plasma renin and serum aldosterone concentrations, reflecting the inhibition of the negative feedback of aldosterone on renin secretion. Appears to have cardioprotective effects in congestive heart failure and left ventricular dysfunction following MI. The cardioprotective action mechanism appears to be related more to the ability of the drug to competitively inhibit the pathophysiologic effects of aldosterone on the myocardium than to its hypotensive effects. Eplerenone reduces coronary vascular inflammation, risk of subsequent development of interstitial myocardial and coronary perivascular fibrosis, cardiac hypertrophy, and/or ventricular remodeling.