The effects of sodium nitroprusside (SNP) on ionic currents in single opossum esophageal circular muscle cells were examined. In voltage clamp, Ca2+ currents were studied after K+ currents were blocked with Cs+ in the patch pipette. The threshold for inward Ca2+ currents was -30 mV with peak current between 0 and +10 mV from holding potentials of -90 mV. The Ca2+ currents had both transient and sustained phases. The transient phase was partially resistant to nifedipine (1 microM). SNP (100 microM) reversibly decreased both the transient and sustained phases of the Ca2+ currents by approximately 20%. In cells dialyzed with high-K+ solutions, voltage-clamp recordings demonstrated the presence of an inward current followed by an outward current at potentials positive to -30 mV. SNP under these conditions resulted in a decrease in the Ca2+ current and decreased the outward current during test depolarizations. Action potentials were evoked during current-clamp recordings that consisted of multiple spikes, depending on the stimulus strength. The threshold for spike generation was close to -30 mV and was blocked by Cd2+, suggesting that the upstroke of the action potential was dependent on Ca2+ influx. SNP significantly attenuated action potentials and produced a small hyperpolarization (5-7 mV). These results suggest that SNP has a direct inhibitory effect on Ca2+ currents and thereby decreases evoked action potentials, and that SNP hyperpolarization is not due to Ca(2+)-activated K+ channels.