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

Yen Yu Lu, Chen Chuan Cheng, Yao Chang Chen, Yung-Kuo Lin, Shih Ann Chen, Yi-Jen Chen

研究成果: 雜誌貢獻文章

17 引文 (Scopus)

摘要

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.
原文英語
頁(從 - 到)781-788
期刊Heart Rhythm
DOIs
出版狀態已發佈 - 2016

指紋

Sinoatrial Node
Hypokalemia
Pulmonary Veins
Hyponatremia
Atrial Fibrillation
Electrolytes
Microelectrodes
Cardiac Myocytes
Potassium
Perfusion
Sodium
Rabbits

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

引用此文

@article{f8e57a5a7c494f40a6414128403b5789,
title = "Electrolyte disturbances differentially regulate sinoatrial node and pulmonary vein electrical activity: A contribution to hypokalemia- or hyponatremia-induced atrial fibrillation",
abstract = "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.",
keywords = "Atrial fibrillation, Hypokalemia, Hyponatremia, Pulmonary vein, Sinoatrial node",
author = "Lu, {Yen Yu} and Cheng, {Chen Chuan} and Chen, {Yao Chang} and Yung-Kuo Lin and Chen, {Shih Ann} and Yi-Jen Chen",
year = "2016",
doi = "10.1016/j.hrthm.2015.12.005",
language = "English",
pages = "781--788",
journal = "Heart Rhythm",
issn = "1547-5271",
publisher = "Elsevier",

}

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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