Angiotensin II and cardiac fibrosis

The renin-angiotensin system has been linked to the pathogenesis of cardiac fibrosis through the use of experimental animal models and by clinical studies. This review emphasizes recent findings implicating the direct action of angiotensin II on cardiac cell types, particularly the cardiac fibroblast, as a causative factor in the development of cardiac fibrosis. The possible influence of other factors acting in concern with angiotensin II either to increase or to attenuate the fibrotic process is also discussed. Nitric oxide is considered as an example of a paracrine agent that can antagonize either the hemodynamic or cellular effects of angiotensin II during both physiological and pathological processes.