Abstract
In the heart, the opening of sarcolemmal ATP-sensitive K + (K ATP) channels seems to be crucial for the cardiac protection against hypoxia/ischaemia. In the present study, we have exposed cardiomyocytes under hypoxia to high extracellular glucose (30 mM). Under these conditions, intracellular concentration of 1,3-bisphosphoglycerate has increased confirming stimulation of glycolysis. Perforated patch–clamp electrophysiology revealed that hypoxia induces whole-cell K + current in cardiomyocytes more efficiently in the presence than in the absence of high glucose. Glucose significantly promoted survival of cardiomyocytes exposed to hypoxia. HMR 1098, an antagonist of sarcolemmal K ATP channels, inhibited glucose-induced activation of whole-cell K + current during hypoxia as well as glucose-mediated cytoprotection. An inhibitor of glyceraldehyde 3-phosphate dehydrogenase, iodoacetate, inhibited glycolysis in hypoxia and blocked the activation of sarcolemmal K ATP channels. Based on the obtained results, we conclude that the activation of sarcolemmal K ATP channels is involved in glucose-mediated cardioprotection.
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