[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 clearly understood. Cellular K+ loss and accumulation of [K+]o may contribute to genesis of malignant ventricular arrhythmia during myocardial ischemia. In the present study, acute hypoxia simply caused a partial decrease in K+ efflux at normal [K+]o, which was not sensitive to glibenclamide (5 x 10(-3) mmol/L). However, at a higher concentration of [K+]o (10.8 mmol/L), the outward K+ current increased dramatically after 10 min hypoxia, which was accompanied with an irreversible hypercontracture and eventual death of the cell. The I-V relation was linear with increasing repolarization, which was blocked by glibenclamide, an antagonist of ATP-sensitive potassium channel. The results suggest that the increased K+ current is ATP-sensitive and is facilitated by accumulation of the [K+]o.