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Extracellular recording was used to study the effect of sodium nitroprusside, a donor of NO, on parameters of action potential and ionic currents in single sciatic nerve fibers and unmyelinated nerve terminals in the sternal muscle in frogs. Sodium nitroprusside significantly decreased the duration of action potential in Ranvier node and the amplitude of afterdepolarization. In motor nerve terminals bathed in low Ca2+ saline, sodium nitroprusside increased phase III amplitude of the nerve terminal response corresponding to outward potas-sium currents. Blockade of voltage-dependent potassium channels with 4-aminopyridine abolished the effects of NO. These data indicate that exogenous NO reduced the duration of action potential and afterdepolarization through enhancement of voltage-dependent potassium currents.