Blocking cardiac ATP-sensitive K+ channels reduces hydroxyl radicals caused by potassium chloride-induced depolarization in the rat myocardium.

摘要: Abstract The current study examined whether opening of the ATP-sensitive K+ (KATP) channel can induce hydroxyl free radical ( OH) generation, as detected by increases in nonenzymatic formation 2,3-dihydroxybenzoic acid (DHBA) levels rat myocardium. When KCl (4–140 mM) was administered to myocardium through microdialysis probe, level 2,3-DHBA increased gradually a potassium ion concentration ([K+]o)-dependent manner. [K+]o for half-maximal effect production (ED50) 67.9 μM. maximum attainable (Emax) 0.171 μM. Induction glibenclamide (10 μM) decreased OH formation. inhibitory (IC50) against (70 mM)-evoked increase 9.2 μM. 5-Hydroxydecanoate (5-HD, 100 μM), another KATP antagonist, also [K+]o-induced IC50 5-HD 107.2 μM. heart subjected myocardial ischemia 15 min occlusion left anterior descending coronary artery (LAD). reperfused, normal elevation dialysate not observed animals pretreated with or (100 μM). These results suggest that cardiac channels depolarization evokes generation.