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Atrial fibrillation is often initiated by bursts of ectopic activity arising in the pulmonary veins. We have previously shown that a 3-h intermittent burst pacing protocol (BPP), mimicking ectopic pulmonary vein foci, shortens action potential duration (APD) locally at the pulmonary vein-atrial interface (PV) while having no effect elsewhere in rabbit atrium. This shortening is Ca(2+) dependent and is prevented by apamin, which blocks small conductance Ca(2+)-activated K(+) channels (SK(Ca)). The present study investigates the ionic and molecular mechanisms whereby two apamin-sensitive SK(Ca) channels, SK2 and SK3, might contribute to the regional APD changes.

Early electrical remodeling in rabbit pulmonary vein results from trafficking of intracellular SK2 channels to membrane sites