Backx P H, Marban E
Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205.
Circ Res. 1993 Apr;72(4):890-900. doi: 10.1161/01.res.72.4.890.
Background outward K+ currents in guinea pig ventricular myocytes were characterized over a broad range of membrane potentials, including those corresponding to the plateau of the action potential. The background current that is blocked by 1 mM Ba2+ (IK,p) activates within 5 msec at positive potentials, does not inactivate, and deactivates very rapidly on repolarization. IK,p is insensitive to Cl- channel blockers, internal or external [Cl-], dihydropyridines, and sulfonylureas. In contrast, the delayed rectifier K+ current (IK) was not completely blocked even by 30 mM Ba2+. Ba(2+)-sensitive current density increased progressively from 0.16 +/- 0.04 pA/pF at 0 mV to 0.52 +/- 0.21 pA/pF at +80 mV (n = 13, mean +/- SEM). The background current remains present when [K+]o is reduced to 0 mM, which suppresses the inward rectifier K+ current (IK1). These and other features suggest that IK,p is generated by K+ channels that are distinct from IK1 or IK. The kinetics and voltage dependence of IK,p render it capable of modulating both the height and duration of the cardiac action potential.
在包括对应动作电位平台期的广泛膜电位范围内，对豚鼠心室肌细胞的背景外向钾电流进行了表征。被1 mM Ba2+阻断的背景电流（IK,p）在正电位下5毫秒内激活，不发生失活，并且在复极化时非常迅速地失活。IK,p对氯离子通道阻滞剂、细胞内或细胞外[Cl-]、二氢吡啶和磺酰脲不敏感。相比之下，即使30 mM Ba2+也不能完全阻断延迟整流钾电流（IK）。Ba(2+)敏感电流密度从0 mV时的0.16±0.04 pA/pF逐渐增加到+80 mV时的0.52±0.21 pA/pF（n = 13，平均值±标准误）。当细胞外[K+]降低到0 mM时，背景电流仍然存在，这抑制了内向整流钾电流（IK1）。这些以及其他特征表明，IK,p是由与IK1或IK不同的钾通道产生的。IK,p的动力学和电压依赖性使其能够调节心脏动作电位的幅度和持续时间。
