A large body of evidence strongly links aldosterone to development and progression of cardiovascular disease, including vascular stiffness, left ventricular hypertrophy, congestive heart failure, chronic kidney disease, and, especially, hypertension. Emerging data suggest that adipocytes may serve as a source of aldosterone, either directly or indirectly, through the release of aldosterone-stimulating factors. If adipocytes are confirmed to have an important contribution to hyperaldosteronism, it would have significant clinical implications in linking aldosterone to obesity-related increases in cardiovascular risk. Such a cause-and-effect situation would then provide the opportunity to reverse that risk with preferential use of aldosterone antagonists in obese patients.
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