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J Appl Physiol 92: 1473-1479, 2002. First published January 4, 2002; doi:10.1152/japplphysiol.00513.2001
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Vol. 92, Issue 4, 1473-1479, April 2002

Exercise training alters an anoxia-induced, glibenclamide-sensitive current in rat ventricular cardiocytes

Korinne N. Jew and Russell L. Moore

Department of Kinesiology and Applied Physiology, University of Colorado Cardiovascular Institute, University of Colorado, Boulder, Colorado 80309-0354

The effect of training on properties of a sarcolemmal ATP-sensitive K+ current (IKATP) was examined in left ventricular cardiocytes isolated from sedentary (Sed) and trained (Tr) female Sprague-Dawley rats. Whole cell patch-clamp techniques were used to characterize IKATP, an anoxia-inducible, glibencamide-sensitive current. An anoxic condition was induced by superfusing cells with a buffer that was equilibrated with 100% N2, maintained under a layer of argon, and that contained 2-deoxy-D-glucose. Over a 1-h period of anoxia, 59% of Tr cells and 85% Sed cells expressed IKATP. In those cells that did express IKATP, the time to expression of the current during the anoxic period occurred significantly later in cells from the Tr group compared with the Sed. Peak IKATP density was significantly lower in the Tr cells compared with the Sed cells. These results indicate that the onset and magnitude of IKATP were altered by training. These alterations in IKATP may be reflective of processes that contribute to training-induced cardioprotection against ischemia-reperfusion damage.

ATP-sensitive K+ current; ATP-sensitive K+ channel; ischemia-reperfusion


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