Abstract
Ca 2+ dynamics and handling in cardiomyocytes are critical for both metabolism and contraction of the heart. Action potentials involve membrane and subcellular components. In response to membrane depolarization during an action potential, L-type Ca 2+ channels open, allowing the influx of Ca 2+ into a restricted subspace where it triggers Ca 2+ release from the sarcoplasmic reticulum (SR) via ryanodine-sensitive Ca 2+ channels (RyRs). This results in a global increase in the cytosolic Ca 2+ concentration which triggers contraction through the contractile proteins. Relaxation follows the reuptake of Ca 2+ into the SR by the Ca 2+ pump in the SR (SERCA) or its extrusion from the cell essentially ensured by the Na–Ca exchanger. A model of Ca 2+ handling model developed in a precedent work give us quite good results but its not sufficient to explain the cell behaviour in presence of some specific substance like arachidonic acid. In order to explain this difference the authors have developed a new model taking into account a modification of some specific components of the SR.
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