| pubmed-article:15935336 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:15935336 | lifeskim:mentions | umls-concept:C0018787 | lld:lifeskim |
| pubmed-article:15935336 | lifeskim:mentions | umls-concept:C0596235 | lld:lifeskim |
| pubmed-article:15935336 | lifeskim:mentions | umls-concept:C0851285 | lld:lifeskim |
| pubmed-article:15935336 | lifeskim:mentions | umls-concept:C0678640 | lld:lifeskim |
| pubmed-article:15935336 | lifeskim:mentions | umls-concept:C1948027 | lld:lifeskim |
| pubmed-article:15935336 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:15935336 | pubmed:dateCreated | 2005-7-11 | lld:pubmed |
| pubmed-article:15935336 | pubmed:abstractText | Cardiac sarcolemmal Na(+)--Ca(2+) exchange is a central component of Ca2+ signaling essential for Ca2+ extrusion and contributing to a variable degree to the development of the systolic Ca2+ transient. Reports on differential gene expression of Na(+)--Ca2+ exchange in cardiac disease and the regulation of its thermodynamic equilibrium depending on intracellular gradients of ion concentrations between subcellular compartments have recently put a new complexion on Na(+)--Ca2+ exchange and its implications for excitation-contraction (E-C) coupling. Heart failure models and genetic approaches to regulate expression of the Na(+)--Ca2+ exchanger have improved our knowledge of exchanger function. Modest overexpression of the Na(+)--Ca2+ exchanger in heterozygous transgenic mice had minimal effects on E-C coupling and cardiac function. However, higher levels of Na(+)--Ca2+ exchange expression in homozygotes led to pathological hypertrophy and failure with an increased interaction between the L-type Ca2+ current and Na(+)--Ca2+ exchange and reduced E-C coupling gain. These results suggested that the Na(+)--Ca2+ exchanger is capable of modulating sarcoplasmic Ca2+ handling and at high expression levels may interact with the gating kinetics of the L-type Ca2+ current by means of regulating subsarcolemmal Ca2+ levels. Despite being a central component in the regulation of cardiac E-C coupling, a newly generated mouse model with cardiac-specific conditional knock-out of the Na(+)--Ca2+ exchanger is viable with unchanged Ca2+ dynamics in adult ventricular myocytes. Cardiac myocytes adapt well to knock-out of the exchanger, apparently by reducing transsarcolemmal fluxes of Ca2+ and increasing E-C coupling gain possibly mediated by changes in submembrane Ca2+ levels. For E-C coupling in the murine model, which relies primarily on sarcoplasmic Ca2+ regulation, this led to the suggestion that the role of Na(+)--Ca2+ exchange should be thought of as a Ca2+ buffering function and not as a major Ca2+ transporter in competition with the sarcoplasmic reticulum. | lld:pubmed |
| pubmed-article:15935336 | pubmed:language | eng | lld:pubmed |
| pubmed-article:15935336 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15935336 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:15935336 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15935336 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15935336 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:15935336 | pubmed:month | Aug | lld:pubmed |
| pubmed-article:15935336 | pubmed:issn | 0008-6363 | lld:pubmed |
| pubmed-article:15935336 | pubmed:author | pubmed-author:SchwingerRobe... | lld:pubmed |
| pubmed-article:15935336 | pubmed:author | pubmed-author:PhilipsonKenn... | lld:pubmed |
| pubmed-article:15935336 | pubmed:author | pubmed-author:ReuterHannesH | lld:pubmed |
| pubmed-article:15935336 | pubmed:author | pubmed-author:HendersonScot... | lld:pubmed |
| pubmed-article:15935336 | pubmed:author | pubmed-author:GoldhaberJosh... | lld:pubmed |
| pubmed-article:15935336 | pubmed:author | pubmed-author:PottChristian... | lld:pubmed |
| pubmed-article:15935336 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:15935336 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:15935336 | pubmed:volume | 67 | lld:pubmed |
| pubmed-article:15935336 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:15935336 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:15935336 | pubmed:pagination | 198-207 | lld:pubmed |
| pubmed-article:15935336 | pubmed:meshHeading | pubmed-meshheading:15935336... | lld:pubmed |
| pubmed-article:15935336 | pubmed:meshHeading | pubmed-meshheading:15935336... | lld:pubmed |
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| pubmed-article:15935336 | pubmed:meshHeading | pubmed-meshheading:15935336... | lld:pubmed |
| pubmed-article:15935336 | pubmed:meshHeading | pubmed-meshheading:15935336... | lld:pubmed |
| pubmed-article:15935336 | pubmed:meshHeading | pubmed-meshheading:15935336... | lld:pubmed |
| pubmed-article:15935336 | pubmed:meshHeading | pubmed-meshheading:15935336... | lld:pubmed |
| pubmed-article:15935336 | pubmed:year | 2005 | lld:pubmed |
| pubmed-article:15935336 | pubmed:articleTitle | Na(+)--Ca2+ exchange in the regulation of cardiac excitation-contraction coupling. | lld:pubmed |
| pubmed-article:15935336 | pubmed:affiliation | Laboratory of Muscle Research and Molecular Cardiology, Department of Internal Medicine III, University of Cologne, Joseph-Stelzmann-Str. 9, 50924 Cologne, Germany. Hannes.Reuter@koeln.de | lld:pubmed |
| pubmed-article:15935336 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:15935336 | pubmed:publicationType | Review | lld:pubmed |
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