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1 Departments of Physiology and 2 Medicine, The University of Western Ontario, and 3 Lawson Research Institute, St. Joseph's Health Centre, London, Ontario, Canada N6A 5C1
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+ (KV) and a Ca2+-dependent K+ (KCa) current. KCa 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 KV current. 4-AP increased resting tension of muscle strips, suggesting a role for KV 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. KV channels participate in regulation of resting tension, whereas the KCa channel limits depolarization and contraction during excitation.
patch clamp; reverse transcriptase-polymerase chain reaction; contraction; Kv1.2; Kv1.5
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