Pulmonary veins contain a myocardial layer, whose electrical activity is considered to be involved in the genesis and maintenance of atrial fibrillation.
To obtain insight into the automaticity of the pulmonary vein myocardium, we studied　the spatio-temporal pattern of the rise in Ca²⁺ during the early phase Ca²⁺ transient of the isolated guinea pig pulmonary vein cardiomyocytes were studied with confocal microscopy.
On induction of Ca²⁺ transients by electrical field stimulation of the pulmonary vein cardiomyocytes, the rise in Ca²⁺ concentration first occurred at the subsarcolemmal region and then spread to the cell interior; this phenomenon was similar to that of atrial but not ventricular cardiomyocytes.
In pulmonary vein cardiomyocytes showing spontaneous activity, the Ca²⁺ transients were preceded by increased firing of Ca²⁺ sparks, which means Ca²⁺ release from sarcoplasmic reticulum. SEA0400, an inhibitor of the Na⁺/Ca²⁺ exchanger, decreased the frequency of the Ca²⁺ transients and eventually inhibited the Ca²⁺ transients completely without decreasing the firing of Ca²⁺ sparks.
In conclusion, the guinea-pig pulmonary vein myocardium has a tendency to show spontaneous electrical activity, which is mediated by Ca²⁺ released from the sarcoplasmic reticulum and the resulting activation of the Na⁺/Ca²⁺ exchanger.