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• W2011032223 abstract "To quantitatively understand intracellular Na+ and Cl− homeostasis as well as roles of Na+/K+ pump and cystic fibrosis transmembrane conductance regulator Cl− channel (ICFTR) during the β1-adrenergic stimulation in cardiac myocyte, we constructed a computer model of β1-adrenergic signaling and implemented it into an excitation-contraction coupling model of the guinea-pig ventricular cell, which can reproduce membrane excitation, intracellular ion changes (Na+, K+, Ca2+ and Cl−), contraction, cell volume, and oxidative phosphorylation. An application of isoproterenol to the model cell resulted in the shortening of action potential duration (APD) after a transient prolongation, the increases in both Ca2+ transient and cell shortening, and the decreases in both Cl− concentration and cell volume. These results are consistent with experimental data. Increasing the density of ICFTR shortened APD and augmented the peak amplitudes of the L-type Ca2+ current (ICaL) and the Ca2+ transient during the β1-adrenergic stimulation. This indirect inotropic effect was elucidated by the increase in the driving force of ICaL via a decrease in plateau potential. Our model reproduced the experimental data demonstrating the decrease in intracellular Na+ during the β-adrenergic stimulation at 0 or 0.5 Hz electrical stimulation. The decrease is attributable to the increase in Na+ affinity of Na+/K+ pump by protein kinase A. However it was predicted that Na+ increases at higher beating rate because of larger Na+ influx through forward Na+/Ca2+ exchange. It was demonstrated that dynamic changes in Na+ and Cl− fluxes remarkably affect the inotropic action of isoproterenol in the ventricular myocytes." @default.
• W2011032223 created "2016-06-24" @default.
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• W2011032223 creator A5074482591 @default.
• W2011032223 date "2008-01-01" @default.
• W2011032223 modified "2023-09-27" @default.
• W2011032223 title "Simulation analysis of intracellular Na+ and Cl− homeostasis during β1-adrenergic stimulation of cardiac myocyte" @default.
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• W2011032223 doi "https://doi.org/10.1016/j.pbiomolbio.2007.07.005" @default.
• W2011032223 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/17826821" @default.
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