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Am J Physiol Heart Circ Physiol (April 18, 2002). doi:10.1152/ajpheart.00107.2002
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Articles in PresS, published online ahead of print April 18, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00107.2002
Submitted on February 8, 2002
Accepted on April 11, 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 Physiology, University of Tennessee, Memphis, TN, USA
2 Cell Biology and Physiology, Washington University, St Louis, MO, USA

* To whom correspondence should be addressed. E-mail: phofmann{at}physio1.utmem.edu.

The functional significance of 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) is 15-20% higher in hearts from transgenics in the absence of cardiac hypertrophy. ß-adrenergic stimulation causes a positive inotropic response from non-transgenics that is not observed in transgenic hearts. Decreasing extracellular Ca2+ decreases LVDP in hearts from non-transgenics, but not in transgenics. These data suggest an increase in intracellular [Ca2+] in transgenic hearts. Additional studies demonstrated hearts from non-transgenic and transgenics have a similar post-ischemic LVDP. However, ischemic preconditioning does not improve post-ischemic recovery in transgenics. Transgenic hearts also demonstrate a poor recovery following 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 leads to hearts which respond poorly to ischemic or metabolic challenges.




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