Trypsin-dispersed cells from hearts (ventricles) of 7 to 8 day chick embryos were cultured 3 to 21 days. The cells became attached to the culture dish and assembled into monolayer communities. By means of a bridge circuit, one microelectrode was used for simultaneously passing current and recording membrane potentials (Vm). The input resistance, calculated by the measured ΔVm for a known step of current, averaged 10 MΩ. Electrotonic depolarization of nonpacemaker cells had no effect on frequency of firing. Within 2 min after addition of Ba++ (5 to 10 mM) to the Tyrode bath, the cells became partially depolarized and quiescent nonpacemaker cells developed oscillations in Vm which led to action potentials. With time, the depolarization became nearly complete and the input resistance increased 2 to 10 times. During such sustained depolarizations, action potentials were no longer produced and often tiny oscillations were observed; however, large action potentials developed during hyperpolarizing pulses. Thus, the automaticity of the depolarized cell became apparent during artificial repolarization. Sr++ (5 to 10 mM) initially produced hyperpolarization and induced automaticity in quiescent nonpacemaker cells. Elevated [K+]o (20 to 30 mM) suppressed automaticity of pacemaker cells and decreased Rm concomitantly. Thus, Ba++ probably converts nonpacemaker cells into pacemaker cells independently of its depolarizing action. Ba++ may induce automaticity and depolarization by decreasing gK, and elevated [K+]o may depress automaticity by increasing gK. The data support the hypothesis that the level of gK determines whether a cell shall function as a pacemaker.

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