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Am J Physiol Heart Circ Physiol 279: H3101-H3112, 2000;
0363-6135/00 $5.00
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Vol. 279, Issue 6, H3101-H3112, December 2000

SPECIAL COMMUNICATION
Cellular and functional defects in a mouse model of heart failure

Giovanni Esposito*,1, L. F. Santana*,2,3,4, Keith Dilly*,3, Jader Dos Santos Cruz3,5, Lan Mao1, W. J. Lederer2,3, and Howard A. Rockman1

1 Department of Medicine, Duke University Medical Center, Durham, North Carolina 27710; 2 Medical Biotechnology Center, University of Maryland Biotechnology Institute, and 3 Department of Physiology, University of Maryland School of Medicine, Baltimore, Maryland 21201; 4 Institute of Neurobiology, University of Puerto Rico, San Juan, Puerto Rico 00901; and 5 Departamento de Bioquimica e Imunologia, Laboratorio de Membranas Excitaveis, Universidade Federal de Minas Gerais, Minas Gerais, Brazil

Heart failure and dilated cardiomyopathy develop in mice that lack the muscle LIM protein (MLP) gene (MLP-/-). The character and extent of the heart failure that occurs in MLP-/- mice were investigated using echocardiography and in vivo pressure-volume (P-V) loop measurements. P-V loop data were obtained with a new method for mice (sonomicrometry) using two pairs of orthogonal piezoelectric crystals implanted in the endocardial wall. Sonomicrometry revealed right-shifted P-V loops in MLP-/- mice, depressed systolic contractility, and additional evidence of heart failure. Cellular changes in MLP-/- mice were examined in isolated single cells using patch-clamp and confocal Ca2+ concentration ([Ca2+]) imaging techniques. This cellular investigation revealed unchanged Ca2+ currents and Ca2+ spark characteristics but decreased intracellular [Ca2+] transients and contractile responses and a defect in excitation-contraction coupling. Normal cellular and whole heart function was restored in MLP-/- mice that express a cardiac-targeted transgene, which blocks the function of beta -adrenergic receptor (beta -AR) kinase-1 (beta ARK1). These data suggest that, despite the persistent stimulus to develop heart failure in MLP-/- mice (i.e., loss of the structural protein MLP), downregulation and desensitization of the beta -ARs may play a pivotal role in the pathogenesis. Furthermore, this work suggests that the inhibition of beta ARK1 action may prove an effective therapy for heart failure.

contractility; beta -adrenergic receptor; excitation-contraction coupling; calcium signaling; transgenic; beta -adrenergic receptor kinase

* G. Esposito, L. F. Santana, and K. Dilly contributed equally to this work.




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