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Augmentation by intracellular ATP of the delayed rectifier current independently of the glibenclamide‐sensitive K‐current in rabbit arterial myocytes

Elevation of intracellular ATP levels by flash photolysis of caged ATP augmented the delayed rectifier K‐current (IKDR) in rabbit pulmonary artery myocytes. The percentage augmentation was unaffected when IKDR was inactivated by 50% (holding potential − 40 mV), although the magnitude of the ATP‐induced current was substantially reduced. Inactivation of 90% IKDR (holding potential − 20 mV) virtually abolished the ATP‐dependent augmentation. We conclude that modulation of IKDR by ATP does not require conversion of the glibenclamide‐sensitive K‐current (IKDR(ATP).