Electrolyte disturbances differentially regulate sinoatrial node and pulmonary vein electrical activity: A contribution to hypokalemia- or hyponatremia-induced atrial fibrillation.

Background: Hypokalemia and hyponatremia increase the occurrence of atrial fibrillation. Sinoatrial nodes (SANs) and pulmonary veins (PVs) play a critical role in the pathophysiology of atrial fibrillation.

Objective: The purpose of this study was to evaluate whether electrolyte disturbances with low concentrations of potassium ([K(+)]) or sodium ([Na(+)]) modulate SAN and PV electrical activity and arrhythmogenesis, and to investigate potential underlying mechanisms.

Methods: Conventional microelectrodes were used to record electrical activity in rabbit SAN and PV tissue preparations before and after perfusion with different low [K(+)] or [Na(+)], interacting with the Na(+)-Ca(2+) exchanger inhibitor KB-R7943 (10 μΜ).

Results: Low [K(+)] (3.5, 3, 2.5, and 2 mM) decreased beating rates in PV cardiomyocytes with genesis of delayed afterdepolarizations (DADs), burst firing, and increased diastolic tension. Low [K(+)] (3.5, 3, 2.5, and 2 mM) also decreased SAN beating rates, with genesis of DADs. Low [Na(+)] increased PV diastolic tension, DADs, and burst firing, which was attenuated in the co-superfusion with low [K(+)] (2 mM). In contrast, low [Na(+)] had little effect on SAN electrical activities. KB-R7943 (10 μΜ) reduced the occurrences of low [K(+)] (2 mM)- or low [Na(+)] (110 mM)-induced DAD and burst firing in both PVs and SANs.

Conclusion: Low [K(+)] and low [Na(+)] differentially modulate SAN and PV electrical properties. Low [K(+)]- or low [Na(+)]-induced slowing of SAN beating rate and genesis of PV burst firing may contribute to the high occurrence of atrial fibrillation during hypokalemia or hyponatremia.