B-Type Natriuretic Peptide Modulates Pulmonary Vein Arrhythmogenesis: A Novel Potential Contributor to the Genesis of Atrial Tachyarrhythmia in Heart Failure

Yung-Kuo Lin, Yao Chang Chen, Yi Ann Chen, Yung Hsin Yeh, Shih Ann Chen, Yi-Jen Chen

研究成果: 雜誌貢獻文章

4 引文 (Scopus)

摘要

Background: Heart failure (HF) plays a critical role in the genesis of atrial fibrillation (AF). A high B-type natriuretic peptide (BNP) level occurs in patients with HF and in patients with AF. However, the role of BNP in the pathophysiology of AF is not clear. The purposes of this study were to evaluate the effects of BNP on pulmonary vein (PV) arrhythmogenesis. Methods and Results: Whole-cell patch clamp and fluorescence were used to study the action potential, ionic currents, and calcium homeostasis in isolated single rabbit PV cardiomyocytes before and after a BNP infusion, with or without ODQ (10 μM), milrinone (50 μM), or ouabain (1 μM). BNP increased PV spontaneous activity by 28.2 ± 7.5% at 100 nM and by 23.8 ± 9.1% at 300 nM. Similar to those with BNP, milrinone 50 μM increased the PV beating rate from 3.0 ± 0.2 to 3.6 ± 0.3 Hz (P < 0.0005, n = 7). In the presence of ODQ application, BNP didn't change PV spontaneous activity. BNP (100 nM) increased calcium transients (F/F0 from 1.6 ± 0.1 to 1.9 ± 0.2, n = 20, P < 0.05) and increased the pacemaker current (0.4 ± 0.1 to 1.0 ± 0.2 pA/pF, n = 17, P < 0.0005) in PV cardiomyocytes. Moreover, BNP (100 nM) increased the transient inward current, sodium currents, sodium-calcium exchanger currents, and L-type calcium current; but reduced late sodium currents and the Na-K pump in PV cardiomyocytes. Conclusion: BNP increases PV arrhythmogenesis, which may contribute to the genesis of atrial tachyarrhythmogenesis in HF. Cyclic GMP activation, phosphodiesterase 3 inhibition and Na+/K+-ATPase inhibition might participate in the BNP modulation of PV electrophysiology.
原文英語
頁(從 - 到)1462-1471
頁數10
期刊Journal of Cardiovascular Electrophysiology
27
發行號12
DOIs
出版狀態已發佈 - 十二月 1 2016

指紋

Pulmonary Veins
Brain Natriuretic Peptide
Tachycardia
Heart Failure
Cardiac Myocytes
Milrinone
Atrial Fibrillation
Calcium
Sodium
Sodium-Calcium Exchanger
Electrophysiology
Cyclic GMP
Phosphoric Diester Hydrolases
Ouabain
Action Potentials
Homeostasis
Fluorescence
Rabbits

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

引用此文

B-Type Natriuretic Peptide Modulates Pulmonary Vein Arrhythmogenesis : A Novel Potential Contributor to the Genesis of Atrial Tachyarrhythmia in Heart Failure. / Lin, Yung-Kuo; Chen, Yao Chang; Chen, Yi Ann; Yeh, Yung Hsin; Chen, Shih Ann; Chen, Yi-Jen.

於: Journal of Cardiovascular Electrophysiology, 卷 27, 編號 12, 01.12.2016, p. 1462-1471.

研究成果: 雜誌貢獻文章

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title = "B-Type Natriuretic Peptide Modulates Pulmonary Vein Arrhythmogenesis: A Novel Potential Contributor to the Genesis of Atrial Tachyarrhythmia in Heart Failure",
abstract = "Background: Heart failure (HF) plays a critical role in the genesis of atrial fibrillation (AF). A high B-type natriuretic peptide (BNP) level occurs in patients with HF and in patients with AF. However, the role of BNP in the pathophysiology of AF is not clear. The purposes of this study were to evaluate the effects of BNP on pulmonary vein (PV) arrhythmogenesis. Methods and Results: Whole-cell patch clamp and fluorescence were used to study the action potential, ionic currents, and calcium homeostasis in isolated single rabbit PV cardiomyocytes before and after a BNP infusion, with or without ODQ (10 μM), milrinone (50 μM), or ouabain (1 μM). BNP increased PV spontaneous activity by 28.2 ± 7.5{\%} at 100 nM and by 23.8 ± 9.1{\%} at 300 nM. Similar to those with BNP, milrinone 50 μM increased the PV beating rate from 3.0 ± 0.2 to 3.6 ± 0.3 Hz (P < 0.0005, n = 7). In the presence of ODQ application, BNP didn't change PV spontaneous activity. BNP (100 nM) increased calcium transients (F/F0 from 1.6 ± 0.1 to 1.9 ± 0.2, n = 20, P < 0.05) and increased the pacemaker current (0.4 ± 0.1 to 1.0 ± 0.2 pA/pF, n = 17, P < 0.0005) in PV cardiomyocytes. Moreover, BNP (100 nM) increased the transient inward current, sodium currents, sodium-calcium exchanger currents, and L-type calcium current; but reduced late sodium currents and the Na-K pump in PV cardiomyocytes. Conclusion: BNP increases PV arrhythmogenesis, which may contribute to the genesis of atrial tachyarrhythmogenesis in HF. Cyclic GMP activation, phosphodiesterase 3 inhibition and Na+/K+-ATPase inhibition might participate in the BNP modulation of PV electrophysiology.",
keywords = "atrial fibrillation, B-type natriuretic peptide, heart failure, pulmonary vein",
author = "Yung-Kuo Lin and Chen, {Yao Chang} and Chen, {Yi Ann} and Yeh, {Yung Hsin} and Chen, {Shih Ann} and Yi-Jen Chen",
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T1 - B-Type Natriuretic Peptide Modulates Pulmonary Vein Arrhythmogenesis

T2 - A Novel Potential Contributor to the Genesis of Atrial Tachyarrhythmia in Heart Failure

AU - Lin, Yung-Kuo

AU - Chen, Yao Chang

AU - Chen, Yi Ann

AU - Yeh, Yung Hsin

AU - Chen, Shih Ann

AU - Chen, Yi-Jen

PY - 2016/12/1

Y1 - 2016/12/1

N2 - Background: Heart failure (HF) plays a critical role in the genesis of atrial fibrillation (AF). A high B-type natriuretic peptide (BNP) level occurs in patients with HF and in patients with AF. However, the role of BNP in the pathophysiology of AF is not clear. The purposes of this study were to evaluate the effects of BNP on pulmonary vein (PV) arrhythmogenesis. Methods and Results: Whole-cell patch clamp and fluorescence were used to study the action potential, ionic currents, and calcium homeostasis in isolated single rabbit PV cardiomyocytes before and after a BNP infusion, with or without ODQ (10 μM), milrinone (50 μM), or ouabain (1 μM). BNP increased PV spontaneous activity by 28.2 ± 7.5% at 100 nM and by 23.8 ± 9.1% at 300 nM. Similar to those with BNP, milrinone 50 μM increased the PV beating rate from 3.0 ± 0.2 to 3.6 ± 0.3 Hz (P < 0.0005, n = 7). In the presence of ODQ application, BNP didn't change PV spontaneous activity. BNP (100 nM) increased calcium transients (F/F0 from 1.6 ± 0.1 to 1.9 ± 0.2, n = 20, P < 0.05) and increased the pacemaker current (0.4 ± 0.1 to 1.0 ± 0.2 pA/pF, n = 17, P < 0.0005) in PV cardiomyocytes. Moreover, BNP (100 nM) increased the transient inward current, sodium currents, sodium-calcium exchanger currents, and L-type calcium current; but reduced late sodium currents and the Na-K pump in PV cardiomyocytes. Conclusion: BNP increases PV arrhythmogenesis, which may contribute to the genesis of atrial tachyarrhythmogenesis in HF. Cyclic GMP activation, phosphodiesterase 3 inhibition and Na+/K+-ATPase inhibition might participate in the BNP modulation of PV electrophysiology.

AB - Background: Heart failure (HF) plays a critical role in the genesis of atrial fibrillation (AF). A high B-type natriuretic peptide (BNP) level occurs in patients with HF and in patients with AF. However, the role of BNP in the pathophysiology of AF is not clear. The purposes of this study were to evaluate the effects of BNP on pulmonary vein (PV) arrhythmogenesis. Methods and Results: Whole-cell patch clamp and fluorescence were used to study the action potential, ionic currents, and calcium homeostasis in isolated single rabbit PV cardiomyocytes before and after a BNP infusion, with or without ODQ (10 μM), milrinone (50 μM), or ouabain (1 μM). BNP increased PV spontaneous activity by 28.2 ± 7.5% at 100 nM and by 23.8 ± 9.1% at 300 nM. Similar to those with BNP, milrinone 50 μM increased the PV beating rate from 3.0 ± 0.2 to 3.6 ± 0.3 Hz (P < 0.0005, n = 7). In the presence of ODQ application, BNP didn't change PV spontaneous activity. BNP (100 nM) increased calcium transients (F/F0 from 1.6 ± 0.1 to 1.9 ± 0.2, n = 20, P < 0.05) and increased the pacemaker current (0.4 ± 0.1 to 1.0 ± 0.2 pA/pF, n = 17, P < 0.0005) in PV cardiomyocytes. Moreover, BNP (100 nM) increased the transient inward current, sodium currents, sodium-calcium exchanger currents, and L-type calcium current; but reduced late sodium currents and the Na-K pump in PV cardiomyocytes. Conclusion: BNP increases PV arrhythmogenesis, which may contribute to the genesis of atrial tachyarrhythmogenesis in HF. Cyclic GMP activation, phosphodiesterase 3 inhibition and Na+/K+-ATPase inhibition might participate in the BNP modulation of PV electrophysiology.

KW - atrial fibrillation

KW - B-type natriuretic peptide

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KW - pulmonary vein

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