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

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F61388998%3A_____%2F02%3A51020084" target="_blank" >RIV/61388998:_____/02:51020084 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/00216224:14110/02:00007136

Výsledek na webu

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DOI - Digital Object Identifier

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Jazyk výsledku

angličtina

Název v původním jazyce

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

Popis výsledku v původním jazyce

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.

Název v anglickém jazyce

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

Popis výsledku anglicky

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.

Druh

J_x - Nezařazeno - Článek v odborném periodiku (Jimp, Jsc a Jost)

CEP obor

BO - Biofyzika

OECD FORD obor

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Projekt

<a href="/cs/project/GP204%2F02%2FD129" target="_blank" >GP204/02/D129: Kvantitativní analýza vlivu tubulárního systému na elektrickou aktivitu srdečních buněk</a><br>

Návaznosti

P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)<br>Z - Vyzkumny zamer (s odkazem do CEZ)

Rok uplatnění

2002

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Scripta Medica

ISSN

1211-3395

e-ISSN

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Svazek periodika

75

Číslo periodika v rámci svazku

4

Stát vydavatele periodika

CZ - Česká republika

Počet stran výsledku

8

Strana od-do

179-186

Kód UT WoS článku

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EID výsledku v databázi Scopus

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