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Am J Physiol Heart Circ Physiol 281: H2539-H2548, 2001;
0363-6135/01 $5.00
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Vol. 281, Issue 6, H2539-H2548, December 2001

Compensatory changes in Ca2+ and myocardial O2 consumption in beta -tropomyosin transgenic hearts

Guy A. MacGowan4, Congwu Du1,3, David F. Wieczorek6, and Alan P. Koretsky1,2,5

1 Pittsburgh Nuclear Magnetic Resonance Center for Biomedical Research, 2 Department of Biological Sciences, and 3 Center for Light Microscope Imaging and Biotechnology, Carnegie Mellon University, Pittsburgh, 15213; 4 Cardiovascular Institute of the University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania 15213; 5 Laboratory of Functional and Molecular Imaging, National Institute of Neurological Disease and Stroke, Bethesda, Maryland 20892; and 6 Department of Molecular Genetics, Biochemistry and Microbiology, University of Cincinnati College of Medicine, Cincinnati, Ohio 45267

Transgenic mice overexpressing beta -tropomyosin have increased myofilament Ca2+ sensitivity that we hypothesized would result in altered relationships among pressure and heart rates, intracellular Ca2+, and myocardial O2 consumption. In perfused hearts from transgenic mice there was a marked negative force-frequency response between 6 and 10 Hz with a 30 ± 3% reduction in peak-positive first derivative of pressure development over time (dP/dt) compared with 14 ± 2% in wild-type mice (P < 0.001). At 8 Hz systolic pressures were normal, though peak systolic intracellular Ca2+ was significantly reduced in transgenic mice versus wild type (726 ± 61 vs. 936 ± 67 nM, P < 0.05) indicating an alteration in the pressure-Ca2+ relationship. Over a wide range of positive and negative inotropic interventions there were normal developed pressures, though marked elevations in myocardial O2 consumption (15-54%). Because pressures are normal and intracellular Ca2+ decreased and myocardial O2 consumption increased, this suggests that these abnormalities are at least in part compensatory mechanisms to the altered myofilament function.

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