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Mechanisms underlying cessation of rabbit sinoatrial node pacemaker activity in high potassium solutions.

To determine the effect of high extracellular potassium concentration ([K]o) on the membrane current of the sinoatrial node cell, voltage clamp experiments were conducted using the double microelectrode technique. When depolarizing clamp pulses were applied, a transient inward current was followed by an outward current and an outward current tail flowed after the pulse. The amplitude of both the transient inward current and the outward current tail were markedly reduced with increasing [K]o, but the magnitude of the outward current during depolarization scarcely changed. The inward current during hyperpolarizing clamp pulses increased in magnitude at higher [K]o and the reversal potential for the inward current change decreased with increasing [K]o. From these results it was concluded that the suppression of the sinoatrial node automaticity at higher [K]o was due to the decrease in magnitude of both the transient inward current and the outward current tail. As the cause of the depression of the transient inward current, its inactivation through depolarization, increased outward leak current and some direct inhibitory effect of K were proposed. The reduction of the outward current tail was attributed to the decrease in the driving force of the K current.