Physiological consequences of transient outward K(+) current activation during heart failure in the canine left ventricle
Research output: Contribution to journal › Journal article › Research › peer-review
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
Original language | English |
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Journal | Journal of Molecular and Cellular Cardiology |
Volume | 52 |
Issue number | 6 |
Pages (from-to) | 1291-8 |
Number of pages | 8 |
ISSN | 0022-2828 |
DOIs | |
Publication status | Published - 2012 |
ID: 38218888