Purpose of review: Aldosterone causes tissue inflammation leading to fibrosis and remodeling in the heart, vasculature, and kidney. We summarize recent data regarding the mechanism(s) through which aldosterone stimulates inflammation.
Recent findings: Studies elucidate the cell-specific effects of mineralocorticoid receptor activation on inflammatory cell infiltration and adhesion, and highlight the role of the macrophage in the development of vascular collagen deposition and hypertension. Activation of nuclear factor-kappaB in vascular smooth muscle cells involves a complex interplay between the angiotensin subtype 1 (AT1) receptor and the mineralocorticoid receptor. Activation of the mineralocorticoid receptor by aldosterone stimulates an inflammatory phenotype in adipocytes and contributes to insulin resistance by increasing oxidative stress.
Summary: Mechanistic studies of aldosterone-induced inflammation provide the rationale for an expanded therapeutic role for mineralocorticoid receptor antagonists and aldosterone synthase inhibitors.