Nitroprusside modulates pulmonary vein arrhythmogenic activity

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

Research output: Contribution to journalArticle

14 Citations (Scopus)

Abstract

Background. Pulmonary veins (PVs) are the most important sources of ectopic beats with the initiation of paroxysmal atrial fibrillation, or the foci of ectopic atrial tachycardia and focal atrial fibrillation. Elimination of nitric oxide (NO) enhances cardiac triggered activity, and NO can decrease PV arrhythmogensis through mechano-electrical feedback. However, it is not clear whether NO may have direct electrophysiological effects on PV cardiomyocytes. This study is aimed to study the effects of nitroprusside (NO donor), on the ionic currents and arrhythmogenic activity of single cardiomyocytes from the PVs. Methods. Single PV cardiomyocytes were isolated from the canine PVs. The action potential and ionic currents were investigated in isolated single canine PV cardiomyocytes before and after sodium nitroprusside (80 M,) using the whole-cell patch clamp technique. Results. Nitroprusside decreased PV cardiomyocytes spontaneous beating rates from 1.7 0.3 Hz to 0.5 0.4 Hz in 9 cells (P <0.05); suppressed delayed afterdepolarization in 4 (80%) of 5 PV cardiomyocytes. Nitroprusside inhibited L-type calcium currents, transient outward currents and transient inward current, but increased delayed rectified potassium currents. Conclusion. Nitroprusside regulates the electrical activity of PV cardiomyocytes, which suggests that NO may play a role in PV arrhythmogenesis.

Original languageEnglish
Article number20
JournalJournal of Biomedical Science
Volume17
Issue number1
DOIs
Publication statusPublished - 2010

Fingerprint

Pulmonary Veins
Nitroprusside
Nitric Oxide
Cardiac Myocytes
Nitric Oxide Donors
Clamping devices
Atrial Fibrillation
Potassium
Canidae
Ectopic Atrial Tachycardia
Calcium
Feedback
Patch-Clamp Techniques
Action Potentials

ASJC Scopus subject areas

  • Clinical Biochemistry
  • Molecular Biology
  • Cell Biology
  • Biochemistry, medical
  • Endocrinology, Diabetes and Metabolism
  • Pharmacology (medical)

Cite this

Nitroprusside modulates pulmonary vein arrhythmogenic activity. / Lin, Yung Kuo; Lu, Yen Yu; Chen, Yao Chang; Chen, Yi Jen; Chen, Shih Ann.

In: Journal of Biomedical Science, Vol. 17, No. 1, 20, 2010.

Research output: Contribution to journalArticle

Lin, Yung Kuo ; Lu, Yen Yu ; Chen, Yao Chang ; Chen, Yi Jen ; Chen, Shih Ann. / Nitroprusside modulates pulmonary vein arrhythmogenic activity. In: Journal of Biomedical Science. 2010 ; Vol. 17, No. 1.
@article{d2f77c8e8b554966bfa02cdb6f39e157,
title = "Nitroprusside modulates pulmonary vein arrhythmogenic activity",
abstract = "Background. Pulmonary veins (PVs) are the most important sources of ectopic beats with the initiation of paroxysmal atrial fibrillation, or the foci of ectopic atrial tachycardia and focal atrial fibrillation. Elimination of nitric oxide (NO) enhances cardiac triggered activity, and NO can decrease PV arrhythmogensis through mechano-electrical feedback. However, it is not clear whether NO may have direct electrophysiological effects on PV cardiomyocytes. This study is aimed to study the effects of nitroprusside (NO donor), on the ionic currents and arrhythmogenic activity of single cardiomyocytes from the PVs. Methods. Single PV cardiomyocytes were isolated from the canine PVs. The action potential and ionic currents were investigated in isolated single canine PV cardiomyocytes before and after sodium nitroprusside (80 M,) using the whole-cell patch clamp technique. Results. Nitroprusside decreased PV cardiomyocytes spontaneous beating rates from 1.7 0.3 Hz to 0.5 0.4 Hz in 9 cells (P <0.05); suppressed delayed afterdepolarization in 4 (80{\%}) of 5 PV cardiomyocytes. Nitroprusside inhibited L-type calcium currents, transient outward currents and transient inward current, but increased delayed rectified potassium currents. Conclusion. Nitroprusside regulates the electrical activity of PV cardiomyocytes, which suggests that NO may play a role in PV arrhythmogenesis.",
author = "Lin, {Yung Kuo} and Lu, {Yen Yu} and Chen, {Yao Chang} and Chen, {Yi Jen} and Chen, {Shih Ann}",
year = "2010",
doi = "10.1186/1423-0127-17-20",
language = "English",
volume = "17",
journal = "Journal of Biomedical Science",
issn = "1021-7770",
publisher = "BioMed Central",
number = "1",

}

TY - JOUR

T1 - Nitroprusside modulates pulmonary vein arrhythmogenic activity

AU - Lin, Yung Kuo

AU - Lu, Yen Yu

AU - Chen, Yao Chang

AU - Chen, Yi Jen

AU - Chen, Shih Ann

PY - 2010

Y1 - 2010

N2 - Background. Pulmonary veins (PVs) are the most important sources of ectopic beats with the initiation of paroxysmal atrial fibrillation, or the foci of ectopic atrial tachycardia and focal atrial fibrillation. Elimination of nitric oxide (NO) enhances cardiac triggered activity, and NO can decrease PV arrhythmogensis through mechano-electrical feedback. However, it is not clear whether NO may have direct electrophysiological effects on PV cardiomyocytes. This study is aimed to study the effects of nitroprusside (NO donor), on the ionic currents and arrhythmogenic activity of single cardiomyocytes from the PVs. Methods. Single PV cardiomyocytes were isolated from the canine PVs. The action potential and ionic currents were investigated in isolated single canine PV cardiomyocytes before and after sodium nitroprusside (80 M,) using the whole-cell patch clamp technique. Results. Nitroprusside decreased PV cardiomyocytes spontaneous beating rates from 1.7 0.3 Hz to 0.5 0.4 Hz in 9 cells (P <0.05); suppressed delayed afterdepolarization in 4 (80%) of 5 PV cardiomyocytes. Nitroprusside inhibited L-type calcium currents, transient outward currents and transient inward current, but increased delayed rectified potassium currents. Conclusion. Nitroprusside regulates the electrical activity of PV cardiomyocytes, which suggests that NO may play a role in PV arrhythmogenesis.

AB - Background. Pulmonary veins (PVs) are the most important sources of ectopic beats with the initiation of paroxysmal atrial fibrillation, or the foci of ectopic atrial tachycardia and focal atrial fibrillation. Elimination of nitric oxide (NO) enhances cardiac triggered activity, and NO can decrease PV arrhythmogensis through mechano-electrical feedback. However, it is not clear whether NO may have direct electrophysiological effects on PV cardiomyocytes. This study is aimed to study the effects of nitroprusside (NO donor), on the ionic currents and arrhythmogenic activity of single cardiomyocytes from the PVs. Methods. Single PV cardiomyocytes were isolated from the canine PVs. The action potential and ionic currents were investigated in isolated single canine PV cardiomyocytes before and after sodium nitroprusside (80 M,) using the whole-cell patch clamp technique. Results. Nitroprusside decreased PV cardiomyocytes spontaneous beating rates from 1.7 0.3 Hz to 0.5 0.4 Hz in 9 cells (P <0.05); suppressed delayed afterdepolarization in 4 (80%) of 5 PV cardiomyocytes. Nitroprusside inhibited L-type calcium currents, transient outward currents and transient inward current, but increased delayed rectified potassium currents. Conclusion. Nitroprusside regulates the electrical activity of PV cardiomyocytes, which suggests that NO may play a role in PV arrhythmogenesis.

UR - http://www.scopus.com/inward/record.url?scp=77950922672&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=77950922672&partnerID=8YFLogxK

U2 - 10.1186/1423-0127-17-20

DO - 10.1186/1423-0127-17-20

M3 - Article

C2 - 20302658

AN - SCOPUS:77950922672

VL - 17

JO - Journal of Biomedical Science

JF - Journal of Biomedical Science

SN - 1021-7770

IS - 1

M1 - 20

ER -