Arrhythmogenic effect of extracellular K-depletion is prevented by the transverse-axial tubular system in a ventricular cardiac cell model
| Autoři | |
|---|---|
| Rok publikování | 2002 |
| Druh | Článek v odborném periodiku |
| Časopis / Zdroj | Scripta Medica Fac.Med.Univ.Masaryk.Brun. |
| Fakulta / Pracoviště MU | |
| Citace | |
| Obor | Fyziologie |
| Klíčová slova | ventricular cell; low external [K]; tubular system; quantitative modelling |
| Popis | In this work, we studied the role of the transverse-axial tubular system (TAT-system) in arrythmogenesis of ventricular cardiac cells under conditions of simulated hypokalaemia (low [K]e). We used the model of a mammalian ventricular myocyte that integrated the quantitative description of electrical activity of surface and tubular membranes and dynamic changes in intracellular ion concentrations. To maintain potassium homeostasis, an energy-dependent K+ extrusion pump was incorporated into the model. According to predictions provided by the model, the TAT-system protects the cell against arrhythmogenesis due to the enhancement of a potassium concentration gradient between tubular and extracellular spaces at low levels of [K]e. The energy-dependent K extrusion pump maintains tubular [K] at a level higher than the overall [K]e. This makes the activation of tubular K-conductances responsible for action potential repolarisation and resting voltage. |
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