Aldosterone mediates cardiac fibrosis in the setting of hypertension.

Cardiac remodeling is a deleterious consequence of arterial hypertension. This remodeling results from cardiac transcriptomic changes induced by mechanical and hormonal factors. Angiotensin II and aldosterone often collaborate in pathological situations to induce hypertrophy of cardiomyocytes, vascular inflammation, perivascular and interstitial fibrosis, and microvascular rarefaction. Experimental models of transgenic mice overexpressing renin in liver, leading to increased plasma angiotensin II and severe hypertension, and mice overexpressing aldosterone-synthase in cardiomyocytes, leading to a doubling of intracardiac aldosterone concentration have shown that cardiac fibrosis in the heart depends on a balance between pro-fibrotic (TGF-ß, galectin-3) and anti-fibrotic (BNP, ANP) factors. Recent studies using cell-specific deletion of the mineralocorticoid receptor indicate that its activation in macrophages is a key step in the development of cardiac fibrosis in the setting of hemodynamic or hormonal challenges. This review focuses on the impact of inappropriate stimulation of aldosterone in the development of cardiac fibrosis.