Evans A M, Clapp L H, Gurney A M
Department of Pharmacology, UMDS, St. Thomas's Hospital, London.
Br J Pharmacol. 1994 Apr;111(4):972-4. doi: 10.1111/j.1476-5381.1994.tb14836.x.
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 (IK(ATP)).
通过笼锁ATP的闪光光解提高细胞内ATP水平，可增强兔肺动脉肌细胞中的延迟整流钾电流（IKDR）。当IKDR被50%失活（钳制电位-40 mV）时，增强的百分比不受影响，尽管ATP诱导电流的幅度大幅降低。IKDR 90%失活（钳制电位-20 mV）实际上消除了ATP依赖性增强。我们得出结论，ATP对IKDR的调节并不需要磺脲类敏感钾电流（IK(ATP)）的转换。
