TRANSIENT OUTWARD CURRENT IN OPOSSUM ESOPHAGEAL CIRCULAR MUSCLE

The whole cell patch-clamp technique was used to record a transient outward K+ current (I-TO) 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. I-TO was recorded at room temperature in the presence of 5 mM internal ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid. Both activation and inactivation kinetics of I-TO were markedly changed when recordings were made at higher temperatures (32 degrees C). I-Aminopyridine (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 I-TO. 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 similar to 8 mV and shifted the upstroke of the action potential to the left. These results indicate that, in the esophageal circular muscle, I-TO is involved in the resting membrane potential and modulation of the onset of action potential.