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Slow Ca2+ sparks de-synchronize Ca2+ release in failing cardiomyocytes: Evidence for altered configuration of Ca2+ release units?

In heart failure, cardiomyocytes exhibit slowing of the rising phase of the Ca2+ transient which contributes to the impaired contractility observed in this condition. We investigated whether alterations in ryanodine receptor function promote slowing of Ca2+ release in a murine model of congestive he...

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Bibliographic Details
Published in:Journal of molecular and cellular cardiology 2013-05, Vol.58, p.41-52
Main Authors: Louch, William E., Hake, Johan, Mørk, Halvor K., Hougen, Karina, Skrbic, Biljana, Ursu, Daniel, Tønnessen, Theis, Sjaastad, Ivar, Sejersted, Ole M.
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Language:English
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Summary:In heart failure, cardiomyocytes exhibit slowing of the rising phase of the Ca2+ transient which contributes to the impaired contractility observed in this condition. We investigated whether alterations in ryanodine receptor function promote slowing of Ca2+ release in a murine model of congestive heart failure (CHF). Myocardial infarction was induced by left coronary artery ligation. When chronic CHF had developed (10weeks post-infarction), cardiomyocytes were isolated from viable regions of the septum. Septal myocytes from SHAM-operated mice served as controls. Ca2+ transients rose markedly slower in CHF than SHAM myocytes with longer time to peak (CHF=152±12% of SHAM, P
ISSN:0022-2828
1095-8584
DOI:10.1016/j.yjmcc.2013.01.014