The whole cell patch-clamp technique was used to record a transient outward K+ current (ITO) from single smooth muscle cells isolated from opossum esophageal circular muscle. The threshold for its activation was -50 mV from holding potentials negative to -70 mV. The current peaked within 10 ms and decayed completely in 200 ms between test depolarization of -40 and -10 mV. ITO was recorded at room temperature in the presence of 5 mM internal ethylene glycol-bis(beta-amino-ethyl ether)-N,N,N',N'-tetraacetic acid. Both activation and inactivation kinetics of ITO were markedly changed when recordings were made at higher temperatures (32 degrees C). 4-Amino-pyridine (4-AP, 3 mM) abolished the fast component of the outward current. Tetraethylammonium ion (TEA, 1-30 mM) reduced the sustained component but did not affect ITO. In the presence of TEA and nifedipine, the voltage dependence of the steady-state inactivation data was well fitted by a Boltzmann distribution with a half-inactivation potential of -57 mV. The half-inactivation potential was shifted to a more positive potential in the presence of Cd2+ (-35 mV). The steady-state inactivation and activation data overlap between -50 and -30 mV, suggesting the presence of a "window" current in this potential range. In current-clamp mode, 4-AP depolarized single esophageal cells by approximately 8 mV and shifted the upstroke of the action potential to the left. These results indicate that, in the esophageal circular muscle, ITO is involved in the resting membrane potential and modulation of the onset of action potential.