Aldosterone and vascular inflammation

Oxidative stress and inflammation contribute to increased cardiovascular morbidity and mortality associated with activation of the renin-angiotensin ( Ang)-aldosterone system ( RAAS). Studies in cultured cells in vitro and in rodent models in vivo demonstrate that aldosterone and/ or mineralocorticoid receptor ( MR) activation cause oxidative stress and vascular inflammation. Translational studies in humans suggest that endogenous aldosterone increases inflammatory biomarkers through an MR-dependent pathway. Clinical studies indicate that the prevalence of hyperaldosteronism may be increased in resistant hypertension,(1) that aldosterone concentrations escape to pretreatment levels during chronic treatment of congestive heart failure or hypertension with an Ang-converting enzyme ( ACE) inhibitor or Ang receptor blocker,(2-4) and that MR antagonism decreases mortality in congestive heart failure. 5,6 This article reviews the current literature regarding mechanism( s) of aldosterone-induced vascular inflammation and its implications for the prevention of vascular injury in humans.