Abstract
Whether sulfonylurea therapy, which blocks ATP-sensitive K + (K ATP) channels, impedes endogenous cardioprotective mechanisms during cellular metabolic impairment remains controversial. Therefore, the effect of glyburide, a prototype sulphonylurea drug, on cytosolic Ca 2+ concentration and K ATP channel activity, was measured in 2-4-dinitrophenol-treated guinea-pig cardiomyocytes, using epifluorescent digital-imaging and cell-attached patch-clamp electrophysiology. Dinitrophenol (200 μM), which uncouples oxidative phosphorylation, induced opening of K ATP channels and Ca 2+ loading. Glyburide (6 μM) which reduced the opening of K ATP channels, aggravated Ca 2+ loading only when applied to dinitrophenol-pretreated myocytes but not when applied with dinitrophenol treatment. We conclude that a blocker of K ATP channels has differential effects upon dinitrophenol-induced intracellular Ca 2+ loading, which appear to depend upon the stage of metabolic insult.
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