title: Angiotensin deficiency in mice leads to dilated cardiomyopathy.
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.
authors.affiliation: Department Cardiology, Campus Benjamin Franklin, Charité Berlin, Hindenburgdamm, Germany. t.walther@erasmusmc.nl
authors.forename: Thomas
authors.initials: T
authors.lastname: Walther
authors.forename: Paul
authors.initials: P
authors.lastname: Steendijk
authors.forename: Dirk
authors.initials: D
authors.lastname: Westermann
authors.forename: Claudia
authors.initials: C
authors.lastname: Hohmann
authors.forename: Karsten
authors.initials: K
authors.lastname: Schulze
authors.forename: Silvia
authors.initials: S
authors.lastname: Heringer-Walther
authors.forename: Heinz-Peter
authors.initials: HP
authors.lastname: Schultheiss
authors.forename: Carsten
authors.initials: C
authors.lastname: Tschöpe
mesh_terms: D000804:Angiotensin II / Q000172:deficiency* / Q000235:genetics; D000808:Angiotensinogen / Q000172:deficiency / Q000235:genetics; D000818:Animals; D002311:Cardiomyopathy, Dilated / Q000175:diagnosis / Q000209:etiology*; D004195:Disease Models, Animal; D004452:Echocardiography / Q000295:instrumentation / Q000379:methods; D006439:Hemodynamics / Q000502:physiology; D007022:Hypotension / Q000209:etiology; D008297:Male; D051379:Mice; D018345:Mice, Knockout; D009426:Netherlands; D011945:Receptors, Angiotensin / Q000502:physiology; D013318:Stroke Volume / Q000502:physiology; D016277:Ventricular Function, Left / Q000502:physiology
chemical_list: D011945:Receptors, Angiotensin; D000808:Angiotensinogen; D000804:Angiotensin II