Delayed rectifier and Ca2+-dependent K+ currents in human esophagus:: roles in regulating muscle contraction

We have examined K+ channels and their function in human esophageal smooth muscle using perforated patch recording, RT-PCR to identify channel mRNA, and muscle contraction to study the effects of channel blockers. Depolarization revealed at least two types of currents: a 4-aminopyridine (4-AP)-sensitive transient delayed rectifier K+ (K-v) and a Ca2+-dependent K+ (K-Ca) current. K-Ca current was active at positive potentials and was blocked by tetraethylammonium (TEA), iberiotoxin, and charybdotoxin but was insensitive to 4-AP. The mRNA encoding the gene products of Kv1.2 and Kv1.5 was identified in muscle and dissociated cells, consistent with these channel types contributing to K-V current. 4-AP increased resting tension of muscle strips, suggesting a role for K-V in setting the membrane potential. TEA, but not 4-AP, augmented the amplitude and duration of electrically evoked contraction, effects that were abolished by nifedipine. Here we provide the first description of macroscopic K+ currents in human esophagus. K-V channels participate in regulation of resting tension, whereas the K-Ca channel limits depolarization and contraction during excitation.