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Am J Physiol Heart Circ Physiol 283: H584-H590, 2002. First published April 18, 2002; doi:10.1152/ajpheart.00107.2002
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Vol. 283, Issue 2, H584-H590, August 2002

Contractility and ischemic response of hearts from transgenic mice with altered sarcolemmal KATP channels

R. Rajashree1, J. C. Koster2, K. P. Markova2, C. G. Nichols2, and P. A. Hofmann1

1 Department of Physiology, University of Tennessee School of Medicine, Memphis, Tennessee 38163; and 2 Department of Cell Biology and Physiology, Washington University School of Medicine, St. Louis, Missouri 63110

The functional significance of ATP-sensitive K+ (KATP) channels is controversial. In the present study, transgenic mice expressing a mutant Kir6.2, with reduced ATP sensitivity, were used to examine the role of sarcolemmal KATP in normal cardiac function and after an ischemic or metabolic challenge. We found left ventricular developed pressure (LVDP) was 15-20% higher in hearts from transgenics in the absence of cardiac hypertrophy. beta -Adrenergic stimulation caused a positive inotropic response from nontransgenic hearts that was not observed in transgenic hearts. Decreasing extracellular Ca2+ decreased LVDP in hearts from nontransgenics but not in those from transgenics. These data suggest an increase in intracellular [Ca2+] in transgenic hearts. Additional studies have demonstrated hearts from nontransgenics and transgenics have a similar postischemic LVDP. However, ischemic preconditioning does not improve postischemic recovery in transgenics. Transgenic hearts also demonstrate a poor recovery after metabolic inhibition. These data are consistent with the hypothesis that sarcolemmal KATP channels are required for development of normal myocardial function, and perturbations of KATP channels lead to hearts that respond poorly to ischemic or metabolic challenges.

ischemic preconditioning; metabolic inhibition; left ventricular developed pressure; heart rate; diastolic pressure; Kir6.2


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