The pulmonary vein myocardium is receiving attention as the source of ectopic electrical activity underlying atrial fibrillation. Electrophysiological and pharmacological analysis in isolated pulmonary vein myocardia from various experimental animal species have revealed that pulmonary vein cardiomyocytes have an intrinsic ability to generate spontaneous action potentials. The spontaneous electrical activity of the pulmonary vein myocardium is accompanied by elevation and oscillation of intracellular Ca
2+ concentration, and the activity of the sarcolemmal Na
+-Ca
2+ exchanger to extrude intracellular Ca
2+ in exchange for three extracellular Na
+ contributes to the diastolic depolarization triggering the action potential. The lower inwardly rectifying repolarizing K
+ current density in the pulmonary vein cardiomyocyte plays a permissive role. Variation in the pattern, waveform and frequency of firing is observed among animal species, which appears to be the result of differences in the type and density of K
+ currents involved in early and late repolarization. Pulmonary vein automaticity is also affected by various neurohumoral substances and pharmacological agents, and by pathological status such as the degree of tissue stretch. Studies on the mechanisms and regulation of pulmonary vein automaticity could lead to the development of novel therapeutic strategies for atrial fibrillation.
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