Resistant hypertension is a common medical disorder. Although the exact incidence of resistant hypertension is not established, estimates derived from recent outcome studies including the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT), Valsartan Antihypertensive Long-term Use Evaluation (VALUE), and Controlled Onset Verapamil Investigation of Cardiovascular End Points (CONVINCE) emphasize that this condition may be more common than previously thought. A major advance in our understanding of the pathogenesis and management of resistant hypertension is the recognition of the importance of aldosterone. Several investigators have postulated a direct role of aldosterone excess as an important mechanism for drug resistance in hypertension. The mechanisms whereby aldosterone elevates BP are complex. It was previously thought that aldosterone produced hypertension primarily by promoting sodium retention with consequent hypervolemia. Recent studies of the effects of aldosterone on vascular smooth muscle have, however, delineated several extrarenal mechanisms whereby aldosterone produces hypertension—primarily by its direct vasoconstrictor effects and by altering vascular compliance. Consequently, aldosterone blockade constitutes an effective intervention for treating resistant hypertension.