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Modelling and measuring electromechanical coupling in the rat heart
Author(s) -
Niederer S. A.,
Ter Keurs H. E. D. J.,
Smith N. P.
Publication year - 2009
Publication title -
experimental physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.925
H-Index - 101
eISSN - 1469-445X
pISSN - 0958-0670
DOI - 10.1113/expphysiol.2008.045880
Subject(s) - troponin c , endoplasmic reticulum , biophysics , troponin , tension (geology) , coupling (piping) , chemistry , electromechanics , myocyte , cardiac muscle , muscle contraction , troponin i , medicine , biochemistry , biology , materials science , physics , thermodynamics , quantum mechanics , myocardial infarction , metallurgy , compression (physics)
Tension‐dependent binding of Ca 2+ to troponin C in the cardiac myocyte has been shown to play an important role in the regulation of Ca 2+ and the activation of tension development. The significance of this regulatory mechanism is quantified experimentally by the quantity of Ca 2+ released following a rapid change in the muscle length. Using a computational, coupled, electromechanics cell model, we have confirmed that the tension dependence of Ca 2+ binding to troponin C, rather than cross‐bridge kinetics or the rate of Ca 2+ uptake by the sarcoplasmic reticulum, determines the quantity of Ca 2+ released following a length step. This cell model has been successfully applied in a continuum model of the papillary muscle to analyse experimental data, suggesting the tension‐dependent binding of Ca 2+ to troponin C as the likely pathway through which the effects of localized impaired tension generation alter the Ca 2+ transient. These experimental results are qualitatively reproduced using a three‐dimensional coupled electromechanics model. Furthermore, the model predicts that changes in the Ca 2+ transient in the viable myocardium surrounding the impaired region are amplified in the absence of tension‐dependent binding of Ca 2+ to troponin C.