Arrhythmogenic effect of extracellular K- depletion is prevented by the transverse-axial tubular system in a ventricular cardiac cell model

0212138 - UT-L 20020084 RIV CZ eng J - Journal Article
Pásek, Michal - Christé, G. - Šimurda, J.
Arrhythmogenic effect of extracellular K- depletion is prevented by the transverse-axial tubular system in a ventricular cardiac cell model.
Scripta Medica. Roč. 75, č. 4 (2002), s. 179-186. ISSN 1211-3395
R&D Projects: GA ČR GP204/02/D129
Institutional research plan: CEZ:AV0Z2076919
Keywords : arrhythmogenic * cardiac
Subject RIV: BO - Biophysics

In this work, we explored quantitatively the significance of the transverse-axial tubular system (TAT-system) for ventricular cell arrhythmogenesis under conditions of simulated hypokalaemia (low [K+]e). We used a model of mammalian ventricular myocyte that integrates the quantitative description of electrical activity of surface and tubular membrane and the dynamic changes of intracellular ion concentrations. The results predict that the TAT-system plays a significant protecting role against cellular arrhythmogenesis that arises from the enhancement of potassium concentration gradient between tubular and extracellular spaces at low levels of [K+]e. An energy-dependent K+ extrusion pump maintains tubular [K+] at a level higher than the overall [K+]e. This sustains the activation of K+ conductances responsible for action potential repolarization and resting voltage.
Permanent Link: http://hdl.handle.net/11104/0107687