rdf:type |
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lifeskim:mentions |
umls-concept:C0030685,
umls-concept:C0034693,
umls-concept:C0034721,
umls-concept:C0036226,
umls-concept:C0205359,
umls-concept:C0205409,
umls-concept:C0242485,
umls-concept:C0391871,
umls-concept:C0456205,
umls-concept:C0596235,
umls-concept:C0680255,
umls-concept:C1283071,
umls-concept:C1550605,
umls-concept:C1963578,
umls-concept:C2339371,
umls-concept:C2348693
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pubmed:dateCreated |
1997-8-8
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pubmed:abstractText |
1. Intracellular calcium concentration ([Ca2+]i) and Na(+)-Ca2+ exchange currents were measured in calcium-overloaded voltage-clamped rat ventricular myocytes loaded with the Ca(2+)-sensitive fluorescent indicator indo-1. Sarcoplasmic reticulum (SR) Ca2+ content was measured from the integral of the caffeine-evoked current. In cells that had spontaneous SR Ca2+ release in 1 mM external Ca2+ concentration ([Ca2+]o)i raising [Ca2+]o increased the frequency of release with no effect on SR Ca2+ content. In quiescent cells, increased [Ca2+]o produced spontaneous Ca2+ release associated with increased SR Ca2+ content. Further increase of [Ca2+]o had no effect on SR Ca2+ content. The amount of Ca2+ leaving the cell during each release was constant over a wide range of frequencies and [Ca2+]o values. It appears there is a maximum level of SR Ca2+ content, perhaps because spontaneous Ca2+ release results when the content reaches a threshold. 2. From the relationship between [Ca2+]i and Na(+)-Ca2+ exchange current during a caffeine response, it is possible to estimate the changes in Na(+)-Ca2+ exchange current expected from a change of [Ca2+]i. The data show that the calcium oscillations contribute a significant fraction of the total extra Ca2+ efflux induced by increasing [Ca2+]o. Raising [Ca2+]o decreased the rate of calcium removal from the cell as measured from the rate of decay of the caffeine response, suggesting that both inhibition of Ca2+ efflux and increased Ca2+ entry account for the Ca2+ overload at elevated [Ca2+]o. 3. Inhibiting spontaneous SR Ca2+ release increases resting [Ca2+]i. The Ca2+ efflux is identical to that in the presence of release. It is concluded that spontaneous release of calcium, although potentially arrhythmogenic, is an effective way to activate Ca2+ efflux in overloaded conditions and minimizes any increase of diastolic tension.
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pubmed:grant |
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/9174989-1610566,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9174989-2213589,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9174989-2261988,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9174989-2307330,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9174989-2443659,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9174989-2451728,
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http://linkedlifedata.com/resource/pubmed/commentcorrection/9174989-2614727,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9174989-2750887,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9174989-3180359,
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http://linkedlifedata.com/resource/pubmed/commentcorrection/9174989-3343586,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9174989-364994,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9174989-3723418,
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http://linkedlifedata.com/resource/pubmed/commentcorrection/9174989-8235594,
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http://linkedlifedata.com/resource/pubmed/commentcorrection/9174989-8620606
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
May
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pubmed:issn |
0022-3751
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
15
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pubmed:volume |
501 ( Pt 1)
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
3-16
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pubmed:dateRevised |
2010-8-25
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pubmed:meshHeading |
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pubmed:year |
1997
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pubmed:articleTitle |
Measurement of sarcoplasmic reticulum Ca2+ content and sarcolemmal Ca2+ fluxes in isolated rat ventricular myocytes during spontaneous Ca2+ release.
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pubmed:affiliation |
Department of Veterinary Preclinical Sciences, University of Liverpool, UK.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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