首页> 美国卫生研究院文献>The Journal of Physiology >A study of pace-maker potential in rabbit sino-atrial node: measurement of potassium activity under voltage-clamp conditions.
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A study of pace-maker potential in rabbit sino-atrial node: measurement of potassium activity under voltage-clamp conditions.

机译:兔窦房结起搏器潜力的研究:在电压钳制条件下测量钾的活性。

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1. A single sucrose-gap voltage-clamp technique was used to control the membrane potential and to measure current in rabbit sino-atrial (SA) strips. K+ activity in the extracellular space was simultaneously measured using K+-selective micro-electrodes. 2. Using double-barrelled K+ selective micro-electrodes it was possible to measure the time course of accumulation or depletion of K+ accompanying a single action potential without complications arising from mechanical or electrical artifacts. 3. K+ activity in the extracellular space increased during the action potential and then decreased to base-line levels during the diastolic depolarization phase. Single beat accumulations of 0.1-0.4 M could be measured. 4. The magnitude of accumulation or depletion of K+ depended upon the membrane potential such that K+ accumulated at potentials positive to -50 mV (K+ efflux greater than K+ uptake) and was depleted from the extracellular space at potentials negative to -50 mV (K+ efflux less than K+ uptake). 5. The rate of K+ depletion was fairly constant during the time course of a clamp step within the range of diastolic depolarization (-55 to -75 mV) even though the accompanying membrane current showed marked time-dependent kinetics. 6. The total membrane conductance measured during the time course of the diastolic depolarization or during the time course of activation of time-dependent 'pace-maker' current remained fairly constant or increased. 7. No reversal potential for the time-dependent 'pace-maker' current could be measured at EK in solutions containing 2.7, 5.4 and 8.1 mM-K+. 8. These results do not support the turn-off a K+ conductance as the primary mechanisms for the generation of the pace-maker potential in SA nodal tissue; rather the results are more consistent with the idea that activation of an inward current, with large positive equilibrium potential, is responsible for pace-making activity.
机译:1.使用单个蔗糖间隙电压钳技术来控制膜电位并测量兔窦房(SA)试纸中的电流。使用K +选择性微电极同时测量细胞外空间中的K +活性。 2.使用双管式K +选择性微电极,可以测量伴随单个动作电位的K +积累或耗竭的时间过程,而不会因机械或电伪像而引起并发症。 3.细胞外空间中的K +活性在动作电位期间增加,然后在舒张期去极化阶段降低至基线水平。可以测量到0.1-0.4 M的单拍累积量。 4. K +的积累或消耗的大小取决于膜电位,使得K +在-50 mV的正电位(K +流出量大于K +摄取)处积累,而在细胞外空间以-50 mV的负电位(K +外排少于K +吸收)。 5.尽管伴随的膜电流显示出明显的时间依赖性动力学,但在钳位步骤的时间过程中,在舒张期去极化(-55至-75 mV)范围内,K +的消耗速率相当恒定。 6.在舒张期去极化的时间过程中或在依赖时间的“起搏器”电流激活的时间过程中测得的总膜电导保持相当恒定或增加。 7.在含有2.7、5.4和8.1 mM-K +的溶液中,在EK不能测量出与时间相关的“起搏器”电流的反向电位。 8.这些结果并不支持关闭K +电导作为在SA淋巴结组织中产生起搏器潜能的主要机制。相反,结果与这样的想法更一致,即具有大的正平衡电位的内向电流的激活负责起搏活动。

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