| First Author | Walther T | Year | 2004 |
| Journal | Eur J Pharmacol | Volume | 493 |
| Issue | 1-3 | Pages | 161-5 |
| PubMed ID | 15189777 | Mgi Jnum | J:101933 |
| Mgi Id | MGI:3605937 | Doi | 10.1016/j.ejphar.2004.04.032 |
| Citation | Walther T, et al. (2004) Angiotensin deficiency in mice leads to dilated cardiomyopathy. Eur J Pharmacol 493(1-3):161-5 |
| abstractText | 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 (tau) 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. |
