See related article, pp 238–244 In the decade since the publication of the Randomized Aldactone Evaluation Study (RALES),1 interest in the role of aldosterone and the mineralocorticoid receptor (MR) has increased exponentially. The comfortable notion that mineralocorticoid hypertension was just a matter of salt and water has been supplanted by a recognition that multiple tissues and systems are impacted.2,3 It is clear that the adverse cardiovascular consequences of mineralocorticoid-induced hypertension are far in excess of what might be expected for the magnitude and duration of the blood pressure rise.4 These observations have focused research on the consequences of MR activation in nonepithelial tissues.5 This represents somewhat of a renaissance as the consequences for the cardiovascular system of exposure to mineralocorticoids was first noted by Hans Seyle in 1946 and rediscovered by Brilla and Weber with further characterization by Young et al.6 These investigators established a robust rodent model of mineralocorticoid-induced hypertension, cardiac hypertrophy, and cardiac fibrosis resulting from mineralocorticoid/salt administration over a period of weeks. The cardiac fibrosis is preceded by vascular inflammation and is independent of the hypertension, cardiac hypertrophy, angiotensin II, and potassium status. It is blocked by coadministration of MR antagonists (spironolactone or eplerenone) and, more importantly, once established, as in RALES, …