Angiotensin deficiency in mice leads to dilated cardiomyopathy
European Journal of Pharmacology , Volume 493 - Issue 1-3 p. 161- 165
To explore the role of angiotensin II, we assessed hemodynamics and cardiac function in angiotensinogen-deficient mice in comparison to wild-type animals. Left ventricular end-diastolic diameter and wall thickness were evaluated by echocardiography and systolic and diastolic left ventricular function by pressure-volume relations using a micro-conductance catheter. Compared to wild-type animals, the angiotensinogen-deficient mice were hypotensive and showed impaired systolic function. The hearts were dilated, demonstrated by echocardiography and by a right-ward shift of the pressure-volume loops, but end-diastolic pressure, isovolumic relaxation (τ) and diastolic stiffness were unchanged. Afterload, however, was reduced leading to maintained cardiac output. Although a blockade of the renin-angiotensin system via angiotensin converting enzyme inhibitors or angiotensin AT1 receptor antagonist is beneficial after cardiac failure, the absence of angiotensin peptides during the ontogenesis leads to dilated cardiomyopathy.
|Angiotensinogen-deficient mice, Cardiac function, Cardiomyopathy, Pressure-volume relation, Renin angiotensin system|
|European Journal of Pharmacology|
|Organisation||Department of Pharmacology|
Walther, T, Steendijk, P, Westermann, D, Hohmann, C, Schulze, K, Heringer-Walther, S, … Tschöpe, C. (2004). Angiotensin deficiency in mice leads to dilated cardiomyopathy. European Journal of Pharmacology, 493(1-3), 161–165. doi:10.1016/j.ejphar.2004.04.032