Background: Stroke is the most serious complication of atrial fibrillation (AF) and mainly caused by atrial contractile dysfunction. Canine atrial cardiomyocytes have constitutively active acetylcholine-regulated potassium current (IKH). Atrial tachycardia (AT) increases it. This study was designed to investigate the role of IKH in atrial contractile dysfunction of the canine. Methods and results: Dogs were divided into 3 groups: (1) unpaced controls (CTLs); (2) short-term AT (SAT) (400 bpm x7-14 days); and (3) long-term AT (LAT) (400 bpm x4-6-weeks). Tertiapin Q-sensitive IKH and calcium transient were recorded in isolated canine atrial cardiomyocytes using whole cell-patch-clamping and confocal microscopy. Atrial contractility changes were recorded with whole left atrial tissue. IKH were significantly increased in SAT and LAT compared with CTLs. At 3 Hz pacing, atrial contractility were significantly decreased in SAT and LAT compared with CTLs (0.47짹0.14 gram in CTLs, 0.18짹0.05 in SAT, 0.03짹0.02 in LAT, p<0.05 compared with CTLs). These changes were significantly increased after highly selective Kir 3 blocker tertiapin Q treatment; 60% in CTLs (p<0.05), 94% in SAT (p<0.05), 256% in LAT (p<0.01). After tertiapin Q infusion in atrial tachycardia groups, significantly increased calcium transient were observed in atrial cardiomyocytes Conclusion: IKH-upregulation is associated with decreased atrial contractility. Tertiapin Q reversed IKH induced atrial contractile dysfunction by increasing calcium transient.