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Am J Physiol Heart Circ Physiol 281: H931-H938, 2001;
0363-6135/01 $5.00
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Vol. 281, Issue 2, H931-H938, August 2001

Cardiac-directed overexpression of wild-type alpha 1B-adrenergic receptor induces dilated cardiomyopathy

Isabelle Lemire1, Anique Ducharme1, Jean-Claude Tardif1, Francine Poulin1, Larry R. Jones2, Bruce G. Allen1, Terence E. Hébert1, and Hansjörg Rindt1

1 Montreal Heart Institute, Research Center, Montreal, Quebec, Canada H1T 1C8; and 2 Krannert Institute of Cardiology, Indiana University School of Medicine, Indianapolis, Indiana 46202

Using transgenesis as a paradigm, we show here that alpha 1-adrenergic receptors (alpha 1AR) play an important role in cardiac homeostasis. Cardiomyocyte-specific overexpression of the alpha 1BAR subtype resulted in the development of dilated cardiomyopathy and death at ~9 mo of age with typical signs of heart failure. Histological analyses showed the enlargement of all four cardiac chambers and cardiomyocyte disarray in the failing hearts. Transgenic animals showed increased left ventricular areas, as assessed by echocardiography. In addition, a progressive decrease in left ventricular systolic function was revealed. The abundance and activity of sarco(endo)plasmic reticulum Ca2+-ATPase (SERCA2) were reduced, and the ratio of phospholamban to SERCA2 was increased. alpha -Myosin heavy chain (MHC) mRNA was less abundant in older transgenic ventricles, whereas beta -MHC was induced in the failing hearts. Titin mRNA abundance was decreased at 9 mo, whereas atrial natriuretic factor mRNA was elevated at all times. This model mimics structural and functional features of idiopathic dilated cardiomyopathy. The results of this study suggest that chronic alpha 1AR activity is deleterious for cardiac function.

heart; transgenic mouse; ventricular dilation; sarco(endo) plasmic proteins; muscle mRNAs


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