Background-We previously characterized a novel K ϩ current (I KH ) with properties of constitutively active acetylcholinerelated current in dog atrium. I KH is sensitive to tertiapin-Q (IC 50 Ϸ10 nmol/L), a highly selective Kir3 current blocker. This study assessed the role of I KH in atrial tachycardia (AT)-remodeled canine left atrium (LA) with the use of tertiapin-Q as a probe. Methods and Results-Dogs were subjected to 7 to 13 days of AT (400 bpm). Coronary-perfused LA preparations were studied intact or subjected to cardiomyocyte isolation. I KH was recorded with patch-clamp methods. AT pacing increased time-dependent hyperpolarization-activated current (I KH ) at Ϫ110 mV from Ϫ1.8Ϯ0.3 (control) to Ϫ3.4Ϯ0.5 pA/pF (AT) and the 100-nmol/L tertiapin-sensitive component from Ϫ1.5Ϯ0.4 (control) to Ϫ3.3Ϯ0.6 pA/pF (AT). Prolonged atrial tachyarrhythmias could be induced with single extrastimuli in AT-remodeled, but not control, preparations, reflecting the atrial fibrillation-promoting effects of AT remodeling. In AT-remodeled preparations, tachyarrhythmia duration averaged 11.0Ϯ5.2 seconds, with a cycle length of 108Ϯ6 ms. Tertiapin-Q decreased tachyarrhythmia duration (to 0.6Ϯ0.1 second; PϽ0.001) and increased tachyarrhythmia cycle length (to 175Ϯ10 ms; PϽ0.001). Atrial action potential duration (APD) was increased 65Ϯ6% by tertiapin in AT-remodeled hearts versus 19Ϯ2% (PϽ0.001) in control. In 2 AT-remodeled preparations, tachyarrhythmia lasted uninterrupted for Ͼ20 minutes; tertiapin-Q slowed and then terminated arrhythmia in both. Tertiapin had no effect on left ventricular cardiomyocyte currents or APD. Conclusions-AT remodeling increases I KH , and a highly selective Kir3 current antagonist, tertiapin-Q, increases APD and suppresses atrial tachyarrhythmias in AT-remodeled preparations without affecting ventricular electrophysiology. Constitutive acetylcholine-related K ϩ current contributes to AT-remodeling effects in dogs and is a potentially interesting antiarrhythmic target.