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Am J Physiol Heart Circ Physiol 280: H569-H575, 2001;
0363-6135/01 $5.00
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Vol. 280, Issue 2, H569-H575, February 2001

Targeted inactivation of Galpha i does not alter cardiac function or beta -adrenergic sensitivity

Mohit Jain1, Chee Chew Lim1, Kohzo Nagata1, Vannessa M. Davis2, David S. Milstone2, Ronglih Liao1, and Richard M. Mortensen3

1 Whitaker Cardiovascular Institute, Boston University School of Medicine, and 2 Vascular Research Division, Department of Pathology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115; and 3 Department of Physiology, University of Michigan, Ann Arbor, Michigan 48109

Inhibitory Galpha i protein increases in the myocardium during hypertrophy and has been associated with beta -adrenergic receptor (beta -AR) desensitization, contractile dysfunction, and progression of cardiac disease. The role of Galpha i proteins in mediating basal cardiac function and beta -AR response in nonpathological myocardium, however, is uncertain. Transgenic mice with targeted inactivation of Galpha i2 or Galpha i3 were examined for in vivo cardiac function with the use of conscious echocardiography and for ex vivo cardiac response to inotropic stimulation with the use of Langendorff blood-perfused isolated hearts and adult ventricular cardiomyocytes. Echocardiography revealed that percent fractional shortening and heart rate were similar among wild-type, Galpha i2-null, and Galpha i3-null mice. Comparable baseline diastolic and contractile performance was also observed in isolated hearts and isolated ventricular myocytes from wild-type mice and mice lacking Galpha i proteins. Isoproterenol infusion enhanced diastolic and contractile performance to a similar degree in wild-type, Galpha i2-null, and Galpha i3-null mice. These data demonstrate no observable role for inhibitory G proteins in mediating basal cardiac function or sensitivity to beta -AR stimulation in nonpathological myocardium.

Gi protein; beta -adrenergic receptor sensitivity; echocardiography; isolated hearts; myocytes


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