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

Abstract

The effect of training on properties of a sarcolemmal ATP-sensitive K+ current (I(K(ATP))) 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 I(K(ATP)), an anoxia-inducible, glibencamide-sensitive current. An anoxic condition was induced by superfusing cells with a buffer that was equilibrated with 100% N(2), 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 I(K(ATP)). In those cells that did express I(K(ATP)), 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 I(K(ATP)) density was significantly lower in the Tr cells compared with the Sed cells. These results indicate that the onset and magnitude of I(K(ATP)) were altered by training. These alterations in I(K(ATP)) may be reflective of processes that contribute to training-induced cardioprotection against ischemia-reperfusion damage.

Myocardial Hsp70 phosphorylation and PKC-mediated cardioprotection following exercise

“…1C), which supports previous reports indicating a role for enhanced mitoK ATP channel function during both early and late phases of cardioprotection (Ockaili et al 1999). Interestingly, exercise-induced alterations in K ATP channels have been reported in cardiomyocytes from trained rats (Jew and Moore 2002), but sarcolemmal rather than mitochondrial K ATP channels appear to be most important in this case (Brown et al 2005a).…”

Perspectives in innate and acquired cardioprotection: cardioprotection acquired through exercise

“…With prior exercise, increased channel density (24,69) may enhance the metabolic sensing capability of the tissue, leading to decreased calcium overload and cell death in the face of cellular ischemia. While purely speculative, such a scheme would also be consistent with observations that exercise has also been shown to delay ischemic contracture (13,15) and the depletion of myocardial ATP during ischemia (35). Clearly much more research in this exciting area is warranted before the mechanisms can be fully elucidated.…”

Mitochondrial KATPchannel inhibition blunts arrhythmia protection in ischemic exercised hearts

“…The precise roles of these ion channels across biochemically diverse physiological scenarios related to IR, however, are not fully understood. Early studies in myocytes from exercised hearts revealed that cardiac K ATP channel opening elicited resistance to anoxic stress, while the nonselective K ATP channel inhibitor, glibenclamide, abolished this protection (28). Follow-up study indicated that exercise stimulated overexpression of the sulfonylurea receptor portion of the sarc K ATP channel promoted protection against IR injury (15).…”