TY - JOUR
T1 - Electrolyte disturbances differentially regulate sinoatrial node and pulmonary vein electrical activity
T2 - A contribution to hypokalemia- or hyponatremia-induced atrial fibrillation
AU - Lu, Yen Yu
AU - Cheng, Chen Chuan
AU - Chen, Yao Chang
AU - Lin, Yung-Kuo
AU - Chen, Shih Ann
AU - Chen, Yi-Jen
PY - 2016
Y1 - 2016
N2 - 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+-Ca2+ 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.
AB - 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+-Ca2+ 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.
KW - Atrial fibrillation
KW - Hypokalemia
KW - Hyponatremia
KW - Pulmonary vein
KW - Sinoatrial node
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U2 - 10.1016/j.hrthm.2015.12.005
DO - 10.1016/j.hrthm.2015.12.005
M3 - Article
C2 - 26654920
AN - SCOPUS:84958918928
SN - 1547-5271
SP - 781
EP - 788
JO - Heart Rhythm
JF - Heart Rhythm
ER -