1. Angiotensin deficiency in mice leads to dilated cardiomyopathy
- Author
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Karsten Schulze, Heinz-Peter Schultheiss, Thomas Walther, Carsten Tschöpe, Paul Steendijk, Dirk Westermann, Claudia Hohmann, Silvia Heringer-Walther, and Internal Medicine
- Subjects
Cardiomyopathy, Dilated ,Male ,Cardiac function curve ,medicine.medical_specialty ,Cardiac output ,Angiotensinogen ,Cardiomyopathy ,Ventricular Function, Left ,Mice ,Afterload ,Internal medicine ,Animals ,Medicine ,Netherlands ,Mice, Knockout ,Pharmacology ,Receptors, Angiotensin ,Angiotensin II receptor type 1 ,biology ,business.industry ,Angiotensin II ,Hemodynamics ,Stroke Volume ,Angiotensin-converting enzyme ,Dilated cardiomyopathy ,medicine.disease ,Disease Models, Animal ,Endocrinology ,Echocardiography ,cardiovascular system ,biology.protein ,Cardiology ,Hypotension ,business - Abstract
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.
- Published
- 2004