Calcium- and voltage-activated plateau currents of cardiac Purkinje fibers.
Calcium- and voltage-activated plateau currents of cardiac Purkinje fibers.
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DOI：
10.1085/jgp.89.6.921
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发表时间：
1987-06
期刊：
影响因子：
--
通讯作者：
Sutko JL
中科院分区：
文献类型：
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作者：
Kenyon JL;Sutko JL
我们已经使用双微电极电压钳技术，调查的组件，有助于形成的早期部分的平台期的动作电位的小牛心脏浦肯野纤维的膜电流。3，4-二氨基吡啶（50 μ M）可降低去极化至-30 mV电位引起的净瞬时外向电流，但对收缩无一致影响。我们将这种效应归因于电压激活的瞬时钾电流成分的阻断。Ryanodine（1 μ M），浦肯野纤维中肌浆网钙释放和细胞内钙振荡的抑制剂（Sutko，J.L.，和J.L.凯尼恩1983.普通生理学杂志。82：385-404），对膜电流具有复杂的影响，因为它消除了阶段性收缩。在去极化的早期（5-30 ms），ryanodine减少了净外向电流。我们将这种效应归因于肌浆网钙释放抑制和细胞内钙瞬变引起的钙激活钾电流成分的丢失。在去极化的后期（50-200 ms），ryanodine增加了净外向电流。在低钠溶液中没有观察到这种效应，我们在-100至+75 mV的电压范围内没有观察到反转电位。这些数据表明，ryanodine对晚膜电流的影响归因于抑制肌浆网钙释放和细胞内钙瞬变引起的钠-钙交换电流的损失。这两种作用的ryanodine是依赖于氯离子，这表明氯离子不携带ryanodine敏感的电流成分。锶（2.7 mM替代钙）和咖啡因（10 mM），干扰肌浆网功能的其他两种治疗方法，与ryanodine有共同的效果。这支持了ryanodine的作用可能归因于抑制肌浆网钙释放的假设。
We have used the two-microelectrode voltage-clamp technique to investigate the components of membrane current that contribute to the formation of the early part of the plateau phase of the action potential of calf cardiac Purkinje fibers. 3,4-Diaminopyridine (50 microM) reduced the net transient outward current elicited by depolarizations to potentials positive to -30 mV but had no consistent effect on contraction. We attribute this effect to the blockade of a voltage-activated transient potassium current component. Ryanodine (1 microM), an inhibitor of sarcoplasmic reticulum calcium release and intracellular calcium oscillations in Purkinje fibers (Sutko, J.L., and J.L. Kenyon. 1983. Journal of General Physiology. 82:385-404), had complex effects on membrane currents as it abolished phasic contractions. At early times during a depolarization (5-30 ms), ryanodine reduced the net outward current. We attribute this effect to the loss of a component of calcium-activated potassium current caused by the inhibition of sarcoplasmic reticulum calcium release and the intracellular calcium transient. At later times during a depolarization (50-200 ms), ryanodine increased the net outward current. This effect was not seen in low-sodium solutions and we could not observe a reversal potential over a voltage range of -100 to +75 mV. These data suggest that the effect of ryanodine on the late membrane current is attributable to the loss of sodium-calcium exchange current caused by the inhibition of sarcoplasmic reticulum calcium release and the intracellular calcium transient. Neither effect of ryanodine was dependent on chloride ions, which suggests that chloride ions do not carry the ryanodine-sensitive current components. Strontium (2.7 mM replacing calcium) and caffeine (10 mM), two other treatments that interfere with sarcoplasmic reticulum function, had effects in common with ryanodine. This supports the hypothesis that the effects of ryanodine may be attributed to the inhibition of sarcoplasmic reticulum calcium release.