%0 Journal Article %1 Lebl_1990_372 %A Leblanc, N. %A Hume, J. R. %D 1990 %J Science %K 1848371 Action Animals, Calcium, Carrier Channels, Conductivity, Contraction, Electric Exchanger, Gallopamil, Gov't, Guinea Myocardial Myocardium, Nisoldipine, Non-U.S. P.H.S., Pigs, Potentials, Proteins, Research Reticulum, Sarcoplasmic Sodium Sodium, Sodium-Calcium Support, Tetrodotoxin, U.S. %N 4953 %P 372--376 %T Sodium current-induced release of calcium from cardiac sarcoplasmic reticulum. %U http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=retrieve&db=pubmed&list_uids=2158146&dopt=Abstract %V 248 %X The role of sodium-calcium exchange at the sarcolemma in the release of calcium from cardiac sarcoplasmic reticulum was investigated in voltage-clamped, isolated cardiac myocytes. In the absence of calcium entry through voltage-dependent calcium channels, membrane depolarization elicited release of calcium from ryanodine-sensitive internal stores. This process was dependent on sodium entry through tetrodotoxin-sensitive sodium channels. Calcium release under these conditions was also dependent on extracellular calcium concentration, suggesting a calcium-induced trigger release mechanism that involves calcium entry into the cell by sodium-calcium exchange. This sodium current-induced calcium release mechanism may explain, in part, the positive inotropic effects of cardiac glycosides and the negative inotropic effects of a variety of antiarrhythmic drugs that interact with cardiac sodium channels. In response to a transient rise of intracellular sodium, sodium-calcium exchange may promote calcium entry into cardiac cells and trigger sarcoplasmic calcium release during physiologic action potentials.

@article{Lebl_1990_372, abstract = {The role of sodium-calcium exchange at the sarcolemma in the release of calcium from cardiac sarcoplasmic reticulum was investigated in voltage-clamped, isolated cardiac myocytes. In the absence of calcium entry through voltage-dependent calcium channels, membrane depolarization elicited release of calcium from ryanodine-sensitive internal stores. This process was dependent on sodium entry through tetrodotoxin-sensitive sodium channels. Calcium release under these conditions was also dependent on extracellular calcium concentration, suggesting a calcium-induced trigger release mechanism that involves calcium entry into the cell by sodium-calcium exchange. This sodium current-induced calcium release mechanism may explain, in part, the positive inotropic effects of cardiac glycosides and the negative inotropic effects of a variety of antiarrhythmic drugs that interact with cardiac sodium channels. In response to a transient rise of intracellular sodium, sodium-calcium exchange may promote calcium entry into cardiac cells and trigger sarcoplasmic calcium release during physiologic action potentials.}, added-at = {2009-06-03T11:20:58.000+0200}, author = {Leblanc, N. and Hume, J. R.}, biburl = {https://www.bibsonomy.org/bibtex/21577d7468d76e8fe06c630527f536970/hake}, description = {The whole bibliography file I use.}, file = {Lebl_1990_372.pdf:Lebl_1990_372.pdf:PDF}, interhash = {83743184a5f5e40bf8d8f22a8fb39810}, intrahash = {1577d7468d76e8fe06c630527f536970}, journal = {Science}, keywords = {1848371 Action Animals, Calcium, Carrier Channels, Conductivity, Contraction, Electric Exchanger, Gallopamil, Gov't, Guinea Myocardial Myocardium, Nisoldipine, Non-U.S. P.H.S., Pigs, Potentials, Proteins, Research Reticulum, Sarcoplasmic Sodium Sodium, Sodium-Calcium Support, Tetrodotoxin, U.S.}, month = Apr, number = 4953, pages = {372--376}, pdf = {Lebl_1990_372.pdf}, pmid = {1848371}, timestamp = {2009-06-03T11:21:19.000+0200}, title = {Sodium current-induced release of calcium from cardiac sarcoplasmic reticulum.}, url = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=retrieve&db=pubmed&list_uids=2158146&dopt=Abstract}, volume = 248, year = 1990 }