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| pubmed-article:11157672 | lifeskim:mentions | umls-concept:C1283071 | lld:lifeskim |
| pubmed-article:11157672 | lifeskim:mentions | umls-concept:C1963578 | lld:lifeskim |
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| pubmed-article:11157672 | lifeskim:mentions | umls-concept:C1708715 | lld:lifeskim |
| pubmed-article:11157672 | lifeskim:mentions | umls-concept:C2346689 | lld:lifeskim |
| pubmed-article:11157672 | lifeskim:mentions | umls-concept:C0439831 | lld:lifeskim |
| pubmed-article:11157672 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:11157672 | pubmed:dateCreated | 2001-2-22 | lld:pubmed |
| pubmed-article:11157672 | pubmed:abstractText | The aim of this study was to investigate how sarcoplasmic reticulum (SR) Ca(2+) content and systolic Ca(2+) are controlled when Ca(2+) entry into the cell is varied. Experiments were performed on voltage-clamped rat and ferret ventricular myocytes loaded with fluo-3 to measure intracellular Ca(2+) concentration ([Ca(2+)](i)). Increasing external Ca(2+) concentration ([Ca(2+)](o)) from 1 to 2 mmol/L increased the amplitude of the systolic Ca(2+) transient with no effect on SR Ca(2+) content. This constancy of SR content is shown to result because the larger Ca(2+) transient activates a larger Ca(2+) efflux from the cell that balances the increased influx. Decreasing [Ca(2+)](o) to 0.2 mmol/L decreased systolic Ca(2+) but produced a small increase of SR Ca(2+) content. This increase of SR Ca(2+) content is due to a decreased release of Ca(2+) from the SR resulting in decreased loss of Ca(2+) from the cell. An increase of [Ca(2+)](o) has two effects: (1) increasing the fraction of SR Ca(2+) content, which is released on depolarization and (2) increasing Ca(2+) entry into the cell. The results of this study show that the combination of these effects results in rapid changes in the amplitude of the systolic Ca(2+) transient. In support of this, the changes of amplitude of the transient occur more quickly following changes of [Ca(2+)](o) than following refilling of the SR after depletion with caffeine. We conclude that the coordinated control of increased Ca(2+) entry and greater fractional release of Ca(2+) is an important factor in regulating excitation-contraction coupling. | lld:pubmed |
| pubmed-article:11157672 | pubmed:language | eng | lld:pubmed |
| pubmed-article:11157672 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11157672 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:11157672 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:11157672 | pubmed:month | Feb | lld:pubmed |
| pubmed-article:11157672 | pubmed:issn | 1524-4571 | lld:pubmed |
| pubmed-article:11157672 | pubmed:author | pubmed-author:EisnerD ADA | lld:pubmed |
| pubmed-article:11157672 | pubmed:author | pubmed-author:DíazM EME | lld:pubmed |
| pubmed-article:11157672 | pubmed:author | pubmed-author:TraffordA WAW | lld:pubmed |
| pubmed-article:11157672 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:11157672 | pubmed:day | 2 | lld:pubmed |
| pubmed-article:11157672 | pubmed:volume | 88 | lld:pubmed |
| pubmed-article:11157672 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:11157672 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:11157672 | pubmed:pagination | 195-201 | lld:pubmed |
| pubmed-article:11157672 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
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| pubmed-article:11157672 | pubmed:year | 2001 | lld:pubmed |
| pubmed-article:11157672 | pubmed:articleTitle | Coordinated control of cell Ca(2+) loading and triggered release from the sarcoplasmic reticulum underlies the rapid inotropic response to increased L-type Ca(2+) current. | lld:pubmed |
| pubmed-article:11157672 | pubmed:affiliation | Unit of Cardiac Physiology, University of Manchester, Manchester, UK.trafford@man.ac.uk | lld:pubmed |
| pubmed-article:11157672 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:11157672 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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