[Effect of acute hypoxia on ATP-sensitive potassium current in ventricular myocytes of guinea-pig].

The role of the ATP-sensitive potassium channel in arrhythmogenesis is not clearlyunderstood. Cellular K+ loss and accumulation of [K+]. may contribute to genesis ofmalignant ventricular arrhythmia during myocardial ischemia. In the present study, acute hypoxia simply caused a partial decrease in K+ efflux at normal [K+], whichwas not sensitive to glibenclamide (5×10-3 mmol/L). However, at a higher concentration of [K+]. (10. 8 mmol/L), the outward K+ current increased dramatically after10 min hypoxia, which was accompanied with an irreversible hypercontracture andeventual death of the cell. The LV relation was linear with increasing repolarization,which was blocked by glibenclamide, an antagonist of ATP-sensitive potussium charrnel. The results suggest that the increased K+ current is ATP-sensitive and is facilitutedby accumulation of the [K+].