Calcium dynamics in cardiac myocytes: a model for drugs effect description

Ca2+ 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 Ca2+ channels open, allowing the influx of Ca2+ into a restricted subspace where it triggers Ca2+ release from the sarcoplasmic reticulum (SR) via ryanodine-sensitive Ca2+ channels (RyRs). This results in a global increase in the cytosolic Ca2+ concentration which triggers contraction through the contractile proteins. Relaxation follows the reuptake of Ca2+ into the SR by the Ca2+ pump in the SR (SERCA) or its extrusion from the cell essentially ensured by the Na–Ca exchanger. A model of Ca2+ 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.