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Ion currents, action potentials, and noradrenergic responses in rat pulmonary vein and left atrial cardiomyocytes.
Physiol Rep. 2020 05; 8(9):e14432.PR

Abstract

The electrophysiological properties of pulmonary vein (PV)-cardiomyocytes, and their responses to the sympathetic neurotransmitter, noradrenaline (NA), are thought to differ from those of the left atrium (LA) and contribute to atrial ectopy. The aim of this study was to examine rat PV cardiomyocyte electrophysiology and responses to NA in comparison with LA cells. LA and PV cardiomyocytes were isolated from adult male Wistar rat hearts, and membrane potentials and ion currents recorded at 36°C using whole-cell patch-clamp techniques. PV and LA cardiomyocytes did not differ in size. In control, there were no differences between the two cell-types in zero-current potential or action potential duration (APD) at 1 Hz, although the incidence of early afterdepolarizations (EADs) was greater in PV than LA cardiomyocytes. The L-type Ca2+ current (ICaL) was ~×1.5 smaller (p = .0029, Student's t test) and the steady-state K+ current (IKss) was ~×1.4 larger (p = .0028, Student's t test) in PV than in LA cardiomyocytes. PV cardiomyocyte inward-rectifier current (IK1) was slightly smaller than LA cardiomyocyte IK1 . In LA cardiomyocytes, NA significantly prolonged APD30 . In PV cells, APD30 responses to 1 μM NA were heterogeneous: while the mean percentage change in APD30 was not different from 0 (16.5 ± 9.7%, n cells/N animals = 12/10, p = .1177, one-sample t test), three cells showed shortening (-18.8 ± 6.0%) whereas nine showed prolongation (28.3 ± 10.1%, p = .008, Student's t test). NA had no effect on IK1 in either cell-type but inhibited PV IKss by 41.9 ± 4.1% (n/N = 23/11 p < .0001), similar to LA cells. NA increased ICaL in most PV cardiomyocytes (median × 2.2-increase, p < .0001, n/N = 32/14, Wilcoxon-signed-rank test), although in 7/32 PV cells ICaL was decreased following NA. PV cardiomyocytes differ from LA cells and respond heterogeneously to NA.

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Authors+Show Affiliations

Cardiovascular Research Laboratories, School of Physiology, Biomedical Sciences Building, University of Bristol, Bristol, UK.

Cardiovascular Research Laboratories, School of Physiology, Biomedical Sciences Building, University of Bristol, Bristol, UK.

Cardiovascular Research Laboratories, School of Physiology, Biomedical Sciences Building, University of Bristol, Bristol, UK.

Cardiovascular Research Laboratories, School of Physiology, Biomedical Sciences Building, University of Bristol, Bristol, UK.

Cardiovascular Research Laboratories, School of Physiology, Biomedical Sciences Building, University of Bristol, Bristol, UK.

MeSH

Action PotentialsAdrenergic alpha-AgonistsAnimalsHeart AtriaIon ChannelsMaleMyocytes, CardiacNorepinephrinePatch-Clamp TechniquesPulmonary VeinsRatsRats, Wistar

Pub Type(s)

Journal Article

Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

32401431

Citation

Bond, Richard C., et al. "Ion Currents, Action Potentials, and Noradrenergic Responses in Rat Pulmonary Vein and Left Atrial Cardiomyocytes." Physiological Reports, vol. 8, no. 9, 2020, pp. e14432.

Bond RC, Choisy SC, Bryant SM, et al. Ion currents, action potentials, and noradrenergic responses in rat pulmonary vein and left atrial cardiomyocytes. Physiol Rep. 2020;8(9):e14432.

Bond, R. C., Choisy, S. C., Bryant, S. M., Hancox, J. C., & James, A. F. (2020). Ion currents, action potentials, and noradrenergic responses in rat pulmonary vein and left atrial cardiomyocytes. Physiological Reports, 8(9), e14432. https://doi.org/10.14814/phy2.14432

Bond RC, et al. Ion Currents, Action Potentials, and Noradrenergic Responses in Rat Pulmonary Vein and Left Atrial Cardiomyocytes. Physiol Rep. 2020;8(9):e14432. PubMed PMID: 32401431.

* Article titles in AMA citation format should be in sentence-case

TY - JOUR T1 - Ion currents, action potentials, and noradrenergic responses in rat pulmonary vein and left atrial cardiomyocytes. AU - Bond,Richard C, AU - Choisy,Stéphanie C, AU - Bryant,Simon M, AU - Hancox,Jules C, AU - James,Andrew F, PY - 2019/09/06/received PY - 2020/04/06/revised PY - 2020/04/10/accepted PY - 2020/5/14/entrez PY - 2020/5/14/pubmed PY - 2021/6/4/medline KW - L-type Ca2+ current (ICaL) KW - action potential KW - delayed afterdepolarization KW - early afterdepolarization KW - inward-rectifier K+ current (IK1) KW - noradrenaline KW - pulmonary vein sleeves KW - steady-state K+ current (IKss) KW - triggered activity SP - e14432 EP - e14432 JF - Physiological reports JO - Physiol Rep VL - 8 IS - 9 N2 - The electrophysiological properties of pulmonary vein (PV)-cardiomyocytes, and their responses to the sympathetic neurotransmitter, noradrenaline (NA), are thought to differ from those of the left atrium (LA) and contribute to atrial ectopy. The aim of this study was to examine rat PV cardiomyocyte electrophysiology and responses to NA in comparison with LA cells. LA and PV cardiomyocytes were isolated from adult male Wistar rat hearts, and membrane potentials and ion currents recorded at 36°C using whole-cell patch-clamp techniques. PV and LA cardiomyocytes did not differ in size. In control, there were no differences between the two cell-types in zero-current potential or action potential duration (APD) at 1 Hz, although the incidence of early afterdepolarizations (EADs) was greater in PV than LA cardiomyocytes. The L-type Ca2+ current (ICaL) was ~×1.5 smaller (p = .0029, Student's t test) and the steady-state K+ current (IKss) was ~×1.4 larger (p = .0028, Student's t test) in PV than in LA cardiomyocytes. PV cardiomyocyte inward-rectifier current (IK1) was slightly smaller than LA cardiomyocyte IK1 . In LA cardiomyocytes, NA significantly prolonged APD30 . In PV cells, APD30 responses to 1 μM NA were heterogeneous: while the mean percentage change in APD30 was not different from 0 (16.5 ± 9.7%, n cells/N animals = 12/10, p = .1177, one-sample t test), three cells showed shortening (-18.8 ± 6.0%) whereas nine showed prolongation (28.3 ± 10.1%, p = .008, Student's t test). NA had no effect on IK1 in either cell-type but inhibited PV IKss by 41.9 ± 4.1% (n/N = 23/11 p < .0001), similar to LA cells. NA increased ICaL in most PV cardiomyocytes (median × 2.2-increase, p < .0001, n/N = 32/14, Wilcoxon-signed-rank test), although in 7/32 PV cells ICaL was decreased following NA. PV cardiomyocytes differ from LA cells and respond heterogeneously to NA. SN - 2051-817X UR - https://www.unboundmedicine.com/medline/citation/32401431/Ion_currents_action_potentials_and_noradrenergic_responses_in_rat_pulmonary_vein_and_left_atrial_cardiomyocytes_ DB - PRIME DP - Unbound Medicine ER -