![]() ![]() IP3 InsP3R automaticity rat pulmonary vein cardiac myocyte α1- and β1-adrenoceptor.īifurcation diagrams of the Ca 2+ dynamics model: ( A) A bifurcation diagram with the total Ca 2+ content within the cell on the abscissa and total amount of Ca 2+ within the junction space ( jnc jnc) on the ordinate (upper) and the corresponding frequency is shown with the same parameter as in the upper panel on the abscissa (bottom) ( B) a bifurcation diagram with the open probability of type II inositol 1,4,5-trisphosphate receptors (pO_InsP 3R) on the abscissa and total amount of Ca 2+ within the jnc ( jnc) on the ordinate (upper) and the corresponding frequency is shown with the same parameter as in the upper panel on the abscissa (bottom). Positive and negative feedback relations were clarified under AP TD generation. Marked and variable latencies initiating AP TDs could be explained by the time courses of the α1- and β1-adrenergic influence on the regulation of intracellular Ca 2+ content and random occurrences of spontaneous TD activating the first AP TD. Under NA effects, repetitive Ca 2+ release from SR triggered spontaneous action potentials (APs) by evoking transient depolarizations (TDs) through Na +/Ca 2+ exchanger (AP TDs). The new PVC model exhibited a resting potential of -68 mV. ![]() Ca 2+ overload in SR increased resting Ca 2+ efflux through the type II inositol 1,4,5-trisphosphate (IP 3) receptors (InsP 3R) as well as ryanodine receptors (RyRs), which finally triggered massive Ca 2+ release through activation of RyRs via local Ca 2+ accumulation in the vicinity of RyRs. We developed a mathematical model of rat PV cardiomyocytes (PVC) based on experimental data that incorporates the microscopic framework of the local control theory of Ca 2+ release from the sarcoplasmic reticulum (SR), which can generate rhythmic Ca 2+ release (limit cycle revealed by the bifurcation analysis) when total Ca 2+ within the cell increased. Cardiomyocytes and myocardial sleeves dissociated from pulmonary veins (PVs) potentially generate ectopic automaticity in response to noradrenaline (NA), and thereby trigger atrial fibrillation. ![]()
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