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.