| pubmed-article:21303662 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:21303662 | lifeskim:mentions | umls-concept:C0225828 | lld:lifeskim |
| pubmed-article:21303662 | lifeskim:mentions | umls-concept:C0021467 | lld:lifeskim |
| pubmed-article:21303662 | lifeskim:mentions | umls-concept:C0021469 | lld:lifeskim |
| pubmed-article:21303662 | lifeskim:mentions | umls-concept:C0596235 | lld:lifeskim |
| pubmed-article:21303662 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
| pubmed-article:21303662 | lifeskim:mentions | umls-concept:C0598002 | lld:lifeskim |
| pubmed-article:21303662 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:21303662 | pubmed:dateCreated | 2011-3-14 | lld:pubmed |
| pubmed-article:21303662 | pubmed:abstractText | (Na(+)+K(+))-ATPase (NKA) mediates positive inotropy in the heart. Extensive studies have demonstrated that the reverse-mode Na(+)/Ca(2+)-exchanger (NCX) plays a critical role in increasing intracellular Ca(2+) concentration through the inhibition of NKA-induced positive inotropy by cardiac glycosides. Little is known about the nature of the NCX functional mode in the activation of NKA-induced positive inotropy. Here, we examined the effect of an NKA activator SSA412 antibody on (45)Ca influx in isolated rat myocytes and found that KB-R7943, a NCX reverse-mode inhibitor, fails to inhibit the activation of NKA-induced (45)Ca influx, suggesting that the Ca(2+) influx via the reverse-mode NCX does not mediate this process. Nifedipine, an L-type Ca(2+) channel (LTCC) inhibitor, completely blocks the activation of NKA-induced (45)Ca influx, suggesting that the LTCC is responsible for the moderate increase in intracellular Ca(2+). In contrast, the inhibition of NKA by ouabain induces 4.7-fold (45)Ca influx compared with the condition of activation of NKA. Moreover, approximately 70% of ouabain-induced (45)Ca influx was obstructed by KB-R7943 and only 30% was impeded by nifedipine, indicating that both the LTCC and the NCX contribute to the rise in intracellular Ca(2+) and that the NCX reverse-mode is the major source for the (45)Ca influx induced by the inhibition of NKA. This study provides direct evidence to demonstrate that the activation of NKA-induced Ca(2+) increase is independent of the reverse-mode NCX and pinpoints a mechanistic distinction between the activation and inhibition of the NKA-mediated Ca(2+) influx path ways in cardiomyocytes. | lld:pubmed |
| pubmed-article:21303662 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21303662 | pubmed:language | eng | lld:pubmed |
| pubmed-article:21303662 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21303662 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:21303662 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21303662 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21303662 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21303662 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21303662 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:21303662 | pubmed:month | Mar | lld:pubmed |
| pubmed-article:21303662 | pubmed:issn | 1090-2104 | lld:pubmed |
| pubmed-article:21303662 | pubmed:author | pubmed-author:ZhangJinJ | lld:pubmed |
| pubmed-article:21303662 | pubmed:author | pubmed-author:ChenLingL | lld:pubmed |
| pubmed-article:21303662 | pubmed:author | pubmed-author:XuKai YKY | lld:pubmed |
| pubmed-article:21303662 | pubmed:author | pubmed-author:XiaoRui-PingR... | lld:pubmed |
| pubmed-article:21303662 | pubmed:author | pubmed-author:DeFilippiChri... | lld:pubmed |
| pubmed-article:21303662 | pubmed:author | pubmed-author:ZhuWeizhongW | lld:pubmed |
| pubmed-article:21303662 | pubmed:copyrightInfo | Copyright © 2011 Elsevier Inc. All rights reserved. | lld:pubmed |
| pubmed-article:21303662 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:21303662 | pubmed:day | 11 | lld:pubmed |
| pubmed-article:21303662 | pubmed:volume | 406 | lld:pubmed |
| pubmed-article:21303662 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:21303662 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:21303662 | pubmed:pagination | 200-3 | lld:pubmed |
| pubmed-article:21303662 | pubmed:meshHeading | pubmed-meshheading:21303662... | lld:pubmed |
| pubmed-article:21303662 | pubmed:meshHeading | pubmed-meshheading:21303662... | lld:pubmed |
| pubmed-article:21303662 | pubmed:meshHeading | pubmed-meshheading:21303662... | lld:pubmed |
| pubmed-article:21303662 | pubmed:meshHeading | pubmed-meshheading:21303662... | lld:pubmed |
| pubmed-article:21303662 | pubmed:meshHeading | pubmed-meshheading:21303662... | lld:pubmed |
| pubmed-article:21303662 | pubmed:meshHeading | pubmed-meshheading:21303662... | lld:pubmed |
| pubmed-article:21303662 | pubmed:meshHeading | pubmed-meshheading:21303662... | lld:pubmed |
| pubmed-article:21303662 | pubmed:meshHeading | pubmed-meshheading:21303662... | lld:pubmed |
| pubmed-article:21303662 | pubmed:meshHeading | pubmed-meshheading:21303662... | lld:pubmed |
| pubmed-article:21303662 | pubmed:year | 2011 | lld:pubmed |
| pubmed-article:21303662 | pubmed:articleTitle | Mechanistic distinction between activation and inhibition of (Na(+)+K(+))-ATPase-mediated Ca2+ influx in cardiomyocytes. | lld:pubmed |
| pubmed-article:21303662 | pubmed:affiliation | Department of Surgery, University of Maryland School of Medicine, Baltimore, MD 21201, USA. kxu002@umaryland.edu | lld:pubmed |
| pubmed-article:21303662 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:21303662 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
| pubmed-article:21303662 | pubmed:publicationType | Research Support, N.I.H., Intramural | lld:pubmed |
