title: Chronic left atrial volume overload abbreviates the action potential duration of the canine pulmonary vein myocardium via activation of IK channel.
abstract: Electrophysiological properties of the pulmonary vein myocardium were assessed in a canine chronic atrioventricular block model resulting in left atrial volume overload. Five chronic atrioventricular block dogs and five sham-operated dogs were used. The heart was removed two months after a surgical procedure causing atrioventricular block, when atrial structural remodeling was established. Standard microelectrode penetrations were made with glass microelectrodes to obtain action potential signals of left atrium and pulmonary vein myocardia. The resting membrane potential in the pulmonary vein was more positive than that in the left atrium (-69 mV vs -74 mV) in both animal groups. The action potential duration at 50% repolarization of the pulmonary vein was shorter in the chronic atrioventricular block dogs than in the sham-operated dogs (38 ms vs 63 ms), whereas no significant difference was detected in the action potential duration of the left atrium between the two animal groups (67 ms vs 61 ms). The action potential duration of the pulmonary vein in the chronic atrioventricular block dogs was prolonged by charybdotoxin but not by iberiotoxin. Such prolongation was not observed in the normal pulmonary vein. These results suggest that long-term left atrial dilatation shortened the action potential duration of pulmonary vein myocardium, which may be associated with activation of the intermediate conductance Ca2+-activated K+ channel (IK channel).
authors.affiliation: Department of Pharmacology, Toho University Faculty of Pharmaceutical Sciences, Funabashi, Chiba 274-8510, Japan.
authors.forename: Hideaki
authors.initials: H
authors.lastname: Nouchi
authors.forename: Akira
authors.initials: A
authors.lastname: Takahara
authors.forename: Hideki
authors.initials: H
authors.lastname: Nakamura
authors.forename: Iyuki
authors.initials: I
authors.lastname: Namekata
authors.forename: Takahiko
authors.initials: T
authors.lastname: Sugimoto
authors.forename: Yayoi
authors.initials: Y
authors.lastname: Tsuneoka
authors.forename: Kiyoshi
authors.initials: K
authors.lastname: Takeda
authors.forename: Toshikazu
authors.initials: T
authors.lastname: Tanaka
authors.forename: Koki
authors.initials: K
authors.lastname: Shigenobu
authors.forename: Atsushi
authors.initials: A
authors.lastname: Sugiyama
authors.forename: Hikaru
authors.initials: H
authors.lastname: Tanaka
mesh_terms: D000200:Action Potentials; D000818:Animals; D016279:Atrial Function, Left / Q000187:drug effects; D054537:Atrioventricular Block / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D018999:Charybdotoxin / Q000494:pharmacology; D002908:Chronic Disease; D004108:Dilatation, Pathologic; D004195:Disease Models, Animal; D004285:Dogs; D006325:Heart Atria / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D051660:Intermediate-Conductance Calcium-Activated Potassium Channels / Q000037:antagonists & inhibitors / Q000378:metabolism*; D009206:Myocardium / Q000378:metabolism*; D010455:Peptides / Q000494:pharmacology; D026902:Potassium Channel Blockers / Q000494:pharmacology; D011667:Pulmonary Veins / Q000187:drug effects / Q000378:metabolism / Q000503:physiopathology*; D013997:Time Factors
chemical_list: D051660:Intermediate-Conductance Calcium-Activated Potassium Channels; D010455:Peptides; D026902:Potassium Channel Blockers; D018999:Charybdotoxin; C064719:iberiotoxin