Physiological consequences of transient outward K(+) current activation during heart failure in the canine left ventricle
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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 journal › Journal article › Research › peer-review
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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