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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
M. Pásek, J. Šimurda, G. Christé,
Jazyk angličtina Země Spojené státy americké
Typ dokumentu časopisecké články
Grantová podpora
NV16-30571A
MZ0
CEP - Centrální evidence projektů
Digitální knihovna NLK
Plný text - Článek
NLK
Free Medical Journals
od 2013
PubMed Central
od 2013
Europe PubMed Central
od 2013
ProQuest Central
od 2013
Open Access Digital Library
od 2001-01-01
Open Access Digital Library
od 2012-12-04
Open Access Digital Library
od 2013-01-01
CINAHL Plus with Full Text (EBSCOhost)
od 2013-01-01
Medline Complete (EBSCOhost)
od 2013-01-01
Health & Medicine (ProQuest)
od 2013
Wiley-Blackwell Open Access Titles
od 2001
ROAD: Directory of Open Access Scholarly Resources
od 2013
PubMed
28321411
DOI
10.1155/2017/6343821
Knihovny.cz E-zdroje
- MeSH
- buněčná membrána metabolismus MeSH
- kardiomyocyty metabolismus MeSH
- krysa rodu rattus MeSH
- membránové potenciály fyziologie MeSH
- modely kardiovaskulární * MeSH
- sodík metabolismus MeSH
- srdeční komory metabolismus MeSH
- vápník metabolismus MeSH
- zvířata MeSH
- Check Tag
- krysa rodu rattus MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
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 Ca(2+) 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 exchangers to higher Ca(2+) transients under the t-tubular membrane. The accompanying rise of Ca(2+) transient was a consequence of a higher Ca(2+) load in sarcoplasmic reticulum induced by the increased Ca(2+) 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.
Department of Physiology Faculty of Medicine Masaryk University Kamenice 5 62500 Brno Czech Republic
Laboratoire de Neurocardiologie EA4612 Université Lyon 1 69003 Lyon France
Citace poskytuje Crossref.org
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