Tsuda Y
Jpn J Physiol. 1979;29(2):103-17. doi: 10.2170/jjphysiol.29.103.
In frog atrium, K depletion exerts initial, and late positive inotropic effects. The initial effect on the membrane potential, current and tension components was studied using a double gap method under voltage clamped and unclamped conditions. In both cases, the presence of the initial effect was demonstrated. The effect was clearer in preparations in which a positive inotropic effect to toxic doses of ouabain (10(-6) M) had already been attained. This suggests that the initial phase is independent from Na-pump inhibition. Voltage clamp study revealed that the slow inward calcium current (ICa) was enhanced transiently after K depletion concomitant with an augmentation of ICa-dependent phasic tension. ICa-independent tonic tension was not altered at this initial phase. For the enhancement of ICa, two mechanisms appeared to be involved, one an enhancement of gCa and the other a faster and/or longer opening of the slow channel. These results indicated that an enhancement of ICa together with the well-known prolongation of action potential were the cause of the initial positive inotropic effect of K depletion.
在蛙心房中,钾离子缺失会产生初始和后期的正性肌力作用。利用双间隙法在电压钳制和非钳制条件下研究了钾离子缺失对膜电位、电流和张力成分的初始影响。在这两种情况下,均证实了初始效应的存在。在对毒剂量哇巴因(10⁻⁶ M)已有正性肌力作用的标本中,这种效应更明显。这表明初始阶段与钠泵抑制无关。电压钳研究显示,钾离子缺失后,慢内向钙电流(ICa)短暂增强,同时依赖ICa的相位性张力增强。在此初始阶段,不依赖ICa的强直性张力未改变。对于ICa的增强,似乎涉及两种机制,一种是gCa的增强,另一种是慢通道更快和/或更长时间的开放。这些结果表明,ICa的增强以及众所周知的动作电位延长是钾离子缺失初始正性肌力作用的原因。