Cardiac fibrosis can be accompanied initially by diastolic and ultimately by systolic ventricular dysfunction. Clinical and experimental evidence suggests a clear association between such adverse structural remodeling and activation of the circulating renin-angiotensin-aldosterone system (RAAS). Infusion of either of two RAAS effector hormones, angiotensin II and aldosterone, in rats evokes perivascular fibrosis of arteries and arterioles of the heart and kidneys. Additionally, increasing evidence indicates locally produced angiotensin II and aldosterone have important paracrine and autocrine actions that play a role in vascular remodeling. Both angiotensin II and aldosterone receptor antagonists have been shown to attenuate the appearance of cardiac and renal fibrosis.
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