Chronic left atrial volume overload abbreviates the action potential duration of the canine pulmonary vein myocardium via activation of IK channel

Impacts of Surgically Performed Renal Denervation on the Cardiovascular and Electrophysiological Variables in the Chronic Atrioventricular Block Dogs – Comparison With Those of Amiodarone Treatment –

“…reported to possess the structural and electrophysiological remodeling that may promote the occurrence and maintenance of atrial fibrillation. 16,[18][19][20] In this study, amiodarone prolonged the AERP, which supports the clinical efficacy of amiodarone in preventing the recurrence of atrial fibrillation. 24 In contrast, renal denervation was reported to reduce the duration of rapid pacing-induced atrial fibrillation in the pig, by which the AERP and P-wave duration were hardly affected.…”

Modulation of Calcium-Activated Potassium Channels Induces Cardiogenesis of Pluripotent Stem Cells and Enrichment of Pacemaker-Like Cells

“…[7][8][9] These channels are found predominantly in the atrium, the atrioventricular node, and pulmonary veins, 8 -10 where they are involved in the regulation of the action potential (AP) duration. 11 In particular, SK4 has been described in atrial stretch-induced atrial natriuretic factor secretion 12 and abbreviation of the AP duration in pulmonary vein myocardium 10 and represents the solely upregulated SK isoform in the developing atrioventricular node. 13 In addition, SK4 was found to be the only SK subtype being upregulated during regeneration/remodeling in a rodent model of myocardial infarction.…”

Pulmonary Vein Myocardium as a Possible Pharmacological Target for the Treatment of Atrial Fibrillation

“…Chronic atrioventricular block is known to produce a moderate degree of sustained volume overload to the atrium (24,25). In our study, whereas the action potential duration of the left atrium was comparable between chronic atrioventricular block dogs and sham animals, that of the pulmonary vein myocardium in the diseased dog was much shorter than that in the sham, which may provide an arrhythmogenic substrate of reentry (26). These results indicate that the pulmonary vein is more sensitive to sustained volume overload than the atrium, leading to generation of a larger pulmonary vein-left atrial difference in action potential duration during the chronic atrioventricular block (Fig.…”

“…The mechanisms of shortened action potential duration in the pulmonary vein of the chronic atrioventricular block dog were analyzed pharmacologically and immunohistologically using peptidic blockers for Ca (26). Since IK channels are generally considered to be abundantly expressed in vascular smooth muscle cells and myofibroblasts as well as immune cells or epithelial tissue especially when they are in the dedifferentiation or proliferating mode (27 -29), the finding may be the first example of its expression in myocardial tissue, suggesting that the pulmonary vein of the atrioventricular block dogs is under remodeling and is shifted towards a dedifferentiated state.…”