Anoxia induces time‐independent K+ current through KATP channels in isolated heart cells of the guinea‐pig.

1. Isolated ventricular heart cells of the guinea‐pig were exposed to anoxia (PO2 < 0.1 Torr) which induced a time‐independent K+ current. This current was studied with the patch clamp technique in the whole‐cell and cell‐attached configuration. 2. The latency until anoxia‐induced changes of whole‐cell current developed was distributed exponentially (mean 10.5 min; n = 41). The current was abolished within 2‐4 s of reoxygenation. 3. The reversal potential of the anoxia‐induced change of whole‐cell current at 5.4 and 15 mM [K+]o was ‐82 and ‐61 mV, respectively. 4. Analysis of current noise in whole‐cell current during the phase of the slow development of the anoxia‐induced current yielded a slope conductance of unitary currents of 8.1 pS (5.4 mM [K+]o) which is far below the 30 pS of KATP channels in inside‐out patches with no Na+ and Mg2+ in the bath. 5. Reduced unitary current induced by anoxia was recorded in single‐channel measurements with 10.4 mM‐K+ in the pipette. 6. Using 150 mM‐K+ in the pipette, anoxia caused unitary inward currents with a slope conductance of 83 pS. The open probability of the channels (P(o)) reached maximum values between 0.6 and 0.95. The channels closed within 1‐3 s of reoxygenation. 7. At voltages between ‐85 and ‐45 mV and maximum P(o), open time histograms were dominated by a fast exponential (tau 01 = 0.55 +/‐ 0.21 ms, mean +/‐ S.D.) and one or two slow exponentials. 8. Voltage ramp experiments showed that single‐channel currents were slightly rectifying in the inward direction. 9. Glibenclamide (1 microM) reversibly blocked the anoxia‐induced whole‐cell and single‐channel currents. 10. It is concluded that during anoxia it is only KATP channels which open by a sufficient decrease of submembrane ATP levels.