U ntil recently, the importance of aldosterone in the development of hypertension has been underestimated and the assumption made that aldosterone-mediated effects could be adequately controlled with angiotensin-converting enzyme (ACE) inhibitors or angiotensin-receptor blockers (ARBs). However, long-term ACE inhibitor or ARB therapy may not adequately protect patients from the effects of aldosterone escape [1][2][3] -an effect that can be minimized by blocking aldosterone at the mineralocorticoid receptor.
4A growing body of clinical evidence has linked aldosterone to the development of hypertension, cardiac hypertrophy, cardiac and vascular fibrosis,
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