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Noninnervated cultured chick embryonic heart cells are depolarized by veratridine (10(-5) 10(-6) g/ml) within a few minutes to membrane potentials of -12 +/- 2 mv. Action potentials and beating cease. Before depolarization begins, the repolarizing phase of the action potential is prolonged and leads to a long-lasting depolarizing afterpotential, probably due to a holding open of Na(+) channels. There is no direct effect on automaticity. Maximum rate of rise of the action potential decreases as a function of the depolarization. The inexcitability is transiently reversed by repolarizing current pulses and by 5 mM Ba(++) (but not Sr(++)) which increases membrane resistance (R(m)) and produces a small transient repolarization. Cocaine does not reverse the depolarization. The depolarization also occurs in Cl(-)-free Ringer and in Na(+)-free Li(+)-Ringer, but not in Na(+)-free sucrose-Ringer. In most cases, R(m), measured in the presence and absence of Cl(-), initially decreases but sometimes increases. Some of the decrease or increase in g(K) may be indirectly produced by anomalous or delayed rectification, respectively. Tetrodotoxin, although having no effect on the action potential magnitude or rate of rise, prevents the depolarizing action of veratridine but not its effect on decreasing R(m). It is concluded that veratridine depolarizes by increasing the resting Na(+) permeability (P(Na)); it also tends to increase P(K), but this action may be obscured by anomalous rectification when E(m) is allowed to change. The equilibrium potential for veratridine action is about halfway between E(Na) and E(K), similar to that of acetylcholine at the vertebrate neuromuscular junction.

Increase in PNa and PK of Cultured Heart Cells Produced by Veratridine