Different Densities of Na-Ca Exchange Current in T-Tubular and Surface Membranes and Their Impact on Cellular Activity in a Model of Rat Ventricular Cardiomyocyte
Identifikátory výsledku
Kód výsledku v IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F61388998%3A_____%2F17%3A00471512" target="_blank" >RIV/61388998:_____/17:00471512 - isvavai.cz</a>
Nalezeny alternativní kódy
RIV/00216224:14110/17:00095655
Výsledek na webu
<a href="http://dx.doi.org/10.1155/2017/6343821" target="_blank" >http://dx.doi.org/10.1155/2017/6343821</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.1155/2017/6343821" target="_blank" >10.1155/2017/6343821</a>
Alternativní jazyky
Jazyk výsledku
angličtina
Název v původním jazyce
Different Densities of Na-Ca Exchange Current in T-Tubular and Surface Membranes and Their Impact on Cellular Activity in a Model of Rat Ventricular Cardiomyocyte
Popis výsledku v původním jazyce
The ratio of densities of Na-Ca exchanger current (INaCa) in the t-tubular and surface membranes (INaCa-ratio) computed from the values of INaCa and membrane capacitances (Cm) measured in adult rat ventricular cardiomyocytes before and after detubulation ranges between 1.7 and 25 (potentially even 40). Variations of action potential waveform and of calcium turnover within this span of the INaCa-ratio were simulated employing previously developed model of rat ventricular cell incorporating separate description of ion transport systems in the t-tubular and surface membranes. The increase of INaCa-ratio from 1.7 to 25 caused a prolongation of APD (duration of action potential at 90% repolarisation) by 12, 9 and 6% and an increase of peak intracellular Ca2+ transient by 45, 19 and 6% at 0.1, 1 and 5 Hz, respectively. The prolonged APD resulted from the increase of INaCa due to the exposure of a larger fraction of Na-Ca transporters to higher Ca2+ transients under t-tubular membrane. The accompanying rise of Ca2+ transient was a consequence of a higher Ca2+ load in sarcoplasmic reticulum induced by the increased Ca2+ cycling between the surface and t-tubular membranes. However, the reason for large differences in the INaCa-ratio assessed from measurements in adult rat cardiomyocytes remains to be explained.
Název v anglickém jazyce
Different Densities of Na-Ca Exchange Current in T-Tubular and Surface Membranes and Their Impact on Cellular Activity in a Model of Rat Ventricular Cardiomyocyte
Popis výsledku anglicky
The ratio of densities of Na-Ca exchanger current (INaCa) in the t-tubular and surface membranes (INaCa-ratio) computed from the values of INaCa and membrane capacitances (Cm) measured in adult rat ventricular cardiomyocytes before and after detubulation ranges between 1.7 and 25 (potentially even 40). Variations of action potential waveform and of calcium turnover within this span of the INaCa-ratio were simulated employing previously developed model of rat ventricular cell incorporating separate description of ion transport systems in the t-tubular and surface membranes. The increase of INaCa-ratio from 1.7 to 25 caused a prolongation of APD (duration of action potential at 90% repolarisation) by 12, 9 and 6% and an increase of peak intracellular Ca2+ transient by 45, 19 and 6% at 0.1, 1 and 5 Hz, respectively. The prolonged APD resulted from the increase of INaCa due to the exposure of a larger fraction of Na-Ca transporters to higher Ca2+ transients under t-tubular membrane. The accompanying rise of Ca2+ transient was a consequence of a higher Ca2+ load in sarcoplasmic reticulum induced by the increased Ca2+ cycling between the surface and t-tubular membranes. However, the reason for large differences in the INaCa-ratio assessed from measurements in adult rat cardiomyocytes remains to be explained.
Klasifikace
Druh
J<sub>imp</sub> - Článek v periodiku v databázi Web of Science
CEP obor
—
OECD FORD obor
10610 - Biophysics
Návaznosti výsledku
Projekt
<a href="/cs/project/NV16-30571A" target="_blank" >NV16-30571A: Klinický význam a elektrofyziologické zhodnocení mutace c.926C>T genu KCNQ1 (p.T309I) jako možné „founder mutation“ syndromu dlouhého intervalu QT</a><br>
Návaznosti
I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace
Ostatní
Rok uplatnění
2017
Kód důvěrnosti údajů
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Údaje specifické pro druh výsledku
Název periodika
BioMed Research International
ISSN
2314-6133
e-ISSN
—
Svazek periodika
2017
Číslo periodika v rámci svazku
2017
Stát vydavatele periodika
US - Spojené státy americké
Počet stran výsledku
9
Strana od-do
—
Kód UT WoS článku
000396222700001
EID výsledku v databázi Scopus
2-s2.0-85016054358