Effects of angiotensin II on cardiac fibroblast contractility

Angiotensin II is known to mediate cardiac remodeling during hypertension by promoting fibrosis and myocyte hypertrophy. This study investigates the effects of angiotensin II on the contractility of the cardiac fibroblast. Using a version of the elastic substratum method, angiotensin II at 1 μM was shown to increase the average traction stress exerted by the cardiac fibroblast up to 75% after one hour of stimulation. The enhanced contractility caused by angiotensin II was eliminated by 1 μM of irbesartan which is a competitive blocker of the AT₁-receptor. Irbesartan not only inhibited the effects of angiotensin II, it actually decreased traction compared to untreated controls. This indicates that the effects of angiotensin II on contractility are mediated at least in part by the AT₁-receptor. Although cardiac fibroblasts are a minor component of the myocardium, a chronic increase in their contractility could be sufficient to increase resistance to ventricular relaxation during diastole, and thereby negatively affect the end-diastolic filling capacity.