Chronic mineralocorticoid (MC) excess, whether due to elevated plasma
aldosterone (ALDO) or deoxycorticosterone (DOC), is associated with a
perivascular fibrosis of systemic and coronary arterioles. This remode
ling of resistance vessels contributes to the appearance of hypertensi
on. Chronic MC excess is also accompanied by cardiac myocyte necrosis,
secondary to myocardial potassium depletion, and a subsequent reparat
ive fibrosis that appears in the normotensive, nonhypertrophied right
and hypertensive, hypertrophied left ventricles. Fibrosis contributes
to the appearance of ventricular arrhythmias and dysfunction. Herein,
clinical and experimental evidence linking chronic, inappropriate (rel
ative to dietary sodium) elevations in circulating ALDO and DOC with t
hese reactive and reparative forms of fibrous tissue formation in the
heart and other tissues is presented.