Physiological consequences of transient outward K(+) current activation during heart failure in the canine left ventricle

Research output: Contribution to journalJournal articleResearchpeer-review

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Physiological consequences of transient outward K(+) current activation during heart failure in the canine left ventricle. / Cordeiro, Jonathan M; Callø, Kirstine; Moise, N Sydney; Kornreich, Bruce; Giannandrea, Dana; Di Diego, José M; Olesen, Søren-Peter; Antzelevitch, Charles.

In: Journal of Molecular and Cellular Cardiology, Vol. 52, No. 6, 2012, p. 1291-8.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Cordeiro, JM, Callø, K, Moise, NS, Kornreich, B, Giannandrea, D, Di Diego, JM, Olesen, S-P & Antzelevitch, C 2012, 'Physiological consequences of transient outward K(+) current activation during heart failure in the canine left ventricle', Journal of Molecular and Cellular Cardiology, vol. 52, no. 6, pp. 1291-8. https://doi.org/10.1016/j.yjmcc.2012.03.001

APA

Cordeiro, J. M., Callø, K., Moise, N. S., Kornreich, B., Giannandrea, D., Di Diego, J. M., Olesen, S-P., & Antzelevitch, C. (2012). Physiological consequences of transient outward K(+) current activation during heart failure in the canine left ventricle. Journal of Molecular and Cellular Cardiology, 52(6), 1291-8. https://doi.org/10.1016/j.yjmcc.2012.03.001

Vancouver

Cordeiro JM, Callø K, Moise NS, Kornreich B, Giannandrea D, Di Diego JM et al. Physiological consequences of transient outward K(+) current activation during heart failure in the canine left ventricle. Journal of Molecular and Cellular Cardiology. 2012;52(6):1291-8. https://doi.org/10.1016/j.yjmcc.2012.03.001

Author

Cordeiro, Jonathan M ; Callø, Kirstine ; Moise, N Sydney ; Kornreich, Bruce ; Giannandrea, Dana ; Di Diego, José M ; Olesen, Søren-Peter ; Antzelevitch, Charles. / Physiological consequences of transient outward K(+) current activation during heart failure in the canine left ventricle. In: Journal of Molecular and Cellular Cardiology. 2012 ; Vol. 52, No. 6. pp. 1291-8.

Bibtex

@article{4f95ff1c0b344b8fb8207a1548dd6eaf,
title = "Physiological consequences of transient outward K(+) current activation during heart failure in the canine left ventricle",
abstract = "Background: Remodeling of ion channel expression is well established in heart failure (HF). We determined the extent to which I(to) is reduced in tachypacing-induced HF and assessed the ability of an I(to) activator (NS5806) to recover this current. Method and results: Whole-cell patch clamp was used to record I(to) in epicardial (Epi) ventricular myocytes. Epi- and endocardial action potentials were recorded from left ventricular wedge preparations. Right ventricular tachypacing-induced heart failure reduced I(to) density in Epi myocytes (Control=22.1±1.9pA/pF vs 16.1±1.4 after 2weeks and 10.7±1.4pA/pF after 5weeks, +50mV). Current decay as well as recovery of I(to) from inactivation progressively slowed with the development of heart failure. Reduction of I(to) density was paralleled by a reduction in phase 1 magnitude, epicardial action potential notch and J wave amplitude recorded from coronary-perfused left ventricular wedge preparations. NS5806 increased I(to) (at +50mV) from 16.1±1.4 to 23.9±2.1pA/pF (p",
author = "Cordeiro, {Jonathan M} and Kirstine Call{\o} and Moise, {N Sydney} and Bruce Kornreich and Dana Giannandrea and {Di Diego}, {Jos{\'e} M} and S{\o}ren-Peter Olesen and Charles Antzelevitch",
note = "Copyright {\textcopyright} 2012 Elsevier Ltd. All rights reserved.",
year = "2012",
doi = "10.1016/j.yjmcc.2012.03.001",
language = "English",
volume = "52",
pages = "1291--8",
journal = "Journal of Molecular and Cellular Cardiology",
issn = "0022-2828",
publisher = "Academic Press",
number = "6",

}

RIS

TY - JOUR

T1 - Physiological consequences of transient outward K(+) current activation during heart failure in the canine left ventricle

AU - Cordeiro, Jonathan M

AU - Callø, Kirstine

AU - Moise, N Sydney

AU - Kornreich, Bruce

AU - Giannandrea, Dana

AU - Di Diego, José M

AU - Olesen, Søren-Peter

AU - Antzelevitch, Charles

N1 - Copyright © 2012 Elsevier Ltd. All rights reserved.

PY - 2012

Y1 - 2012

N2 - Background: Remodeling of ion channel expression is well established in heart failure (HF). We determined the extent to which I(to) is reduced in tachypacing-induced HF and assessed the ability of an I(to) activator (NS5806) to recover this current. Method and results: Whole-cell patch clamp was used to record I(to) in epicardial (Epi) ventricular myocytes. Epi- and endocardial action potentials were recorded from left ventricular wedge preparations. Right ventricular tachypacing-induced heart failure reduced I(to) density in Epi myocytes (Control=22.1±1.9pA/pF vs 16.1±1.4 after 2weeks and 10.7±1.4pA/pF after 5weeks, +50mV). Current decay as well as recovery of I(to) from inactivation progressively slowed with the development of heart failure. Reduction of I(to) density was paralleled by a reduction in phase 1 magnitude, epicardial action potential notch and J wave amplitude recorded from coronary-perfused left ventricular wedge preparations. NS5806 increased I(to) (at +50mV) from 16.1±1.4 to 23.9±2.1pA/pF (p

AB - Background: Remodeling of ion channel expression is well established in heart failure (HF). We determined the extent to which I(to) is reduced in tachypacing-induced HF and assessed the ability of an I(to) activator (NS5806) to recover this current. Method and results: Whole-cell patch clamp was used to record I(to) in epicardial (Epi) ventricular myocytes. Epi- and endocardial action potentials were recorded from left ventricular wedge preparations. Right ventricular tachypacing-induced heart failure reduced I(to) density in Epi myocytes (Control=22.1±1.9pA/pF vs 16.1±1.4 after 2weeks and 10.7±1.4pA/pF after 5weeks, +50mV). Current decay as well as recovery of I(to) from inactivation progressively slowed with the development of heart failure. Reduction of I(to) density was paralleled by a reduction in phase 1 magnitude, epicardial action potential notch and J wave amplitude recorded from coronary-perfused left ventricular wedge preparations. NS5806 increased I(to) (at +50mV) from 16.1±1.4 to 23.9±2.1pA/pF (p

U2 - 10.1016/j.yjmcc.2012.03.001

DO - 10.1016/j.yjmcc.2012.03.001

M3 - Journal article

C2 - 22434032

VL - 52

SP - 1291

EP - 1298

JO - Journal of Molecular and Cellular Cardiology

JF - Journal of Molecular and Cellular Cardiology

SN - 0022-2828

IS - 6

ER -

ID: 38218888