%0 Journal Article %1 Sipi_2007_339 %A Sipido, Karin R %A Bito, V. %A Antoons, G. %A Volders, Paul G %A Vos, Marc A %D 2007 %J Ann N Y Acad Sci %K Arrhythmias, Cardiac, Exchanger, Heart Humans; Sodium-Calcium Ventricles, physiology physiopathology; %P 339--348 %R 10.1196/annals.1387.066 %T Na/Ca exchange and cardiac ventricular arrhythmias. %U http://dx.doi.org/10.1196/annals.1387.066 %V 1099 %X 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.

@article{Sipi_2007_339, 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.}, added-at = {2009-06-03T11:20:58.000+0200}, author = {Sipido, Karin R and Bito, V. and Antoons, G. and Volders, Paul G and Vos, Marc A}, biburl = {https://www.bibsonomy.org/bibtex/24724fd19467b736e4c7c3bf15f7ba3f5/hake}, description = {The whole bibliography file I use.}, doi = {10.1196/annals.1387.066}, file = {Sipi_2007_339.pdf:Sipi_2007_339.pdf:PDF}, institution = {Laboratory of Experimental Cardiology, KUL, Campus Gasthuisberg O/N1, 704, Herestraat 49, B-3000 Leuven, Belgium. Karin.Sipido@med.kuleuven.be}, interhash = {65850e013d78aa9d985a3a96873f6169}, intrahash = {4724fd19467b736e4c7c3bf15f7ba3f5}, journal = {Ann N Y Acad Sci}, keywords = {Arrhythmias, Cardiac, Exchanger, Heart Humans; Sodium-Calcium Ventricles, physiology physiopathology;}, month = Mar, pages = {339--348}, pdf = {Sipi_2007_339.pdf}, pii = {1099/1/339}, pmid = {17446474}, timestamp = {2009-06-03T11:21:30.000+0200}, title = {Na/Ca exchange and cardiac ventricular arrhythmias.}, url = {http://dx.doi.org/10.1196/annals.1387.066}, volume = 1099, year = 2007 }