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SHR Neuro Cancer Cardio Lipid Metab Microb

Sipido, KR; Bito, V; Antoons, G; Volders, PG; Vos, MA.
Na/Ca exchange and cardiac ventricular arrhythmias.
Ann N Y Acad Sci. 2007; 1099(6 Suppl):339-348 Doi: 10.1196/annals.1387.066
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Co-authors Med Uni Graz
Antoons Gudrun
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Abstract:
Ventricular arrhythmias are a major cause of death in cardiovascular disease. Ca2+ removal from the cell by the electrogenic Na/Ca exchanger is essential for the Ca2+ flux balance during excitation-contraction coupling but also contributes to the electrical events. "Classic" views on the exchanger in arrhythmias include its well-recognized role as depolarizing current underlying delayed afterdepolarizations (DADs) during spontaneous Ca2+ release and the alterations in expression in certain forms of cardiac hypertrophy and heart failure. "Novel" views relate to more subtle roles for the exchanger in arrhythmias. Na/Ca exchange function in disease could be modulated indirectly, through phosphorylation or anchoring proteins. Ongoing studies relate Na/Ca exchange to variability in action potential duration (APD) and early afterdepolarizations (EADs) in a dog model of cardiac hypertrophy and arrhythmias. Further research on drugs that target Na/Ca exchange will have to carefully examine the effects on Ca2+ balance.
Find related publications in this database (using NLM MeSH Indexing)
Arrhythmias, Cardiac - physiopathology
Heart Ventricles - physiopathology
Humans -
Sodium-Calcium Exchanger - physiology

Find related publications in this database (Keywords)
cardiac myocytes
arrhythmia
Na/Ca exchange
calcium
delayed after depolarizations
calcium channel
sarcoplasmic reticulum
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