A growing body of preclinical and clinical evidence has demonstrated that mineralocorticoids, especially aldosterone, are intimately involved in the development of target organ injury in all major target organs of hypertensive disease, and that pharmacological inhibition of mineralocorticoids, or adrenalectomy markedly reduces myocardial injury, stroke and renal vascular disease. Animal studies demonstrated that aldosterone/salt treatment induces inflammatory remodeling of coronary and renal arteries with associated ischemic and necrotic lesions. These mineralocorticoid/salt-induced inflammatory changes are usually associated with activation of oxidative stress in vascular cells as well as the expression and progressive upregulation of proinflammatory mediators such as osteopontin, MCP-1, COX-2 and NF-kB. Importantly, the activation of proinflammatory mediators has been shown to be diminished and vascular and cardiac pathology reduced by aldosterone inhibition, implicating a role for these hormones in the progression of inflammatory injury in target tissues. In clinical studies, aldosterone antagonism has also been shown to provide significant end-organ protection in the heart and kidney. Indeed, this strategy has proven to be effective to improve endothelial dysfunction in hypertensive patients and to reduce cardiovascular morbidity and mortality in patients with congestive heart failure or left ventricular dysfunction following a myocardial infarction. Whether this benefits are related to inhibition of aldosterone-induced vascular inflammatory changes is yet to be documented. Thus, an increasing body of evidence now indicates that aldosterone antagonism may be a key therapeutic strategy for the treatment of hypertension and cardiovascular disease.