Intracellular recordings were taken from the smooth muscle of the guinea pig trachea, and the effects of intrinsic nerve stimulation were examined. Approximately 50% of the cells had stable resting membrane potentials of 50 ± 1 mV. The remaining cells displayed spontaneous oscillations in membrane potential, which were abolished either by blocking voltage-dependent Ca²⁺ channels with nifedipine or by depleting intracellular Ca²⁺ stores with ryanodine. In quiescent cells, stimulation with a single impulse evoked an excitatory junction potential (EJP). In 30% of these cells, trains of stimuli evoked an EJP that was followed by oscillations in membrane potential. Transmural nerve stimulation caused an increase in the frequency of spontaneous oscillations. All responses were abolished by the muscarinic-receptor antagonist hyoscine (1 µM). In quiescent cells, nifedipine (1 µM) reduced EJPs by 30%, whereas ryanodine (10 µM) reduced EJPs by 93%. These results suggest that both the release of Ca²⁺ from intracellular stores and the influx of Ca²⁺ through voltage-dependent Ca²⁺ channels are important determinants of spontaneous and nerve-evoked electrical activity of guinea pig tracheal smooth muscle.