Klitzner T, Morad M
Pflugers Arch. 1983 Sep;398(4):267-73. doi: 10.1007/BF00657236.
The effect of Ni2+ on E-C coupling events of the frog ventricular muscle were studied using a single sucrose gap voltage clamp technique. The results showed that Ni2+ increased the overshoot potential and depressed and prolonged the plateau of the action potential. Ni2+ also increased the dependence of the overshoot potential on [Na]0 from 18 to 58 mV per decade. In the presence of Ni2+, TTX blocked both the upstroke and the plateau of the action potential. The combination of TTX and Ni2+ suppressed the tension-voltage relation, the time-dependent outward currents and K+ efflux. While suppression of the tension-voltage relation by Ni2+ alone was reversed by increasing [Ca]0, the effects of Ni2+ plus TTX are not reversed by addition of Ca2+. The results suggest that Ni2+ may alter the action potential by slowing the inactivation of the Na+ current and blocking the inward Ca2+ current. Although the tension-suppressant effects of Ni2+ could be attributed to the inhibition of a slowly inactivating Ca2+ current, the effects of Ni2+ in the presence of TTX were less readily explained. Several possible mechanisms are considered which are all consistent with the hypothesis that development of tension in ventricular strips is mediated by both a Ca2+ current and a Ca2+ counter-transport system.
采用单蔗糖间隙电压钳技术研究了Ni2+对蛙心室肌电-机械偶联事件的影响。结果表明，Ni2+增加了超射电位，降低并延长了动作电位的平台期。Ni2+还使超射电位对[Na]0的依赖性从每十倍浓度变化18 mV增加到58 mV。在存在Ni2+的情况下，TTX阻断了动作电位的上升支和平台期。TTX和Ni2+的组合抑制了张力-电压关系、时间依赖性外向电流和K+外流。虽然单独的Ni2+对张力-电压关系的抑制可通过增加[Ca]0来逆转，但添加Ca2+并不能逆转Ni2+加TTX的作用。结果表明，Ni2+可能通过减慢Na+电流的失活和阻断内向Ca2+电流来改变动作电位。虽然Ni2+的张力抑制作用可能归因于对缓慢失活的Ca2+电流的抑制，但Ni2+在存在TTX时的作用较难解释。文中考虑了几种可能的机制，这些机制均与心室条带中张力的产生由Ca2+电流和Ca2+逆向转运系统介导的假说一致。
