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rdf:type |
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lifeskim:mentions |
umls-concept:C0018787,
umls-concept:C0034693,
umls-concept:C0034721,
umls-concept:C0036226,
umls-concept:C0085979,
umls-concept:C0242485,
umls-concept:C0456205,
umls-concept:C0596235,
umls-concept:C1511572,
umls-concept:C1550548,
umls-concept:C1550605,
umls-concept:C1555714,
umls-concept:C1705654,
umls-concept:C2339371
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pubmed:issue |
3
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pubmed:dateCreated |
1997-5-5
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pubmed:abstractText |
This study investigates the contribution of Ca2+ entry via sarcolemmal (SL) Ca2+ channels to the Ca2+ transient and its relationship with sarcoplasmic reticulum (SR) Ca2+ content during steady-state contraction in guinea pig and rat ventricular myocytes. The action potential clamp technique was used to obtain physiologically relevant changes in membrane potential. A method is shown that allows calculation of Ca2+ entry through the SL Ca2+ channels by measuring Cd(2+)-sensitive current during the whole cardiac cycle. SR Ca2+ content was calculated from caffeine-induced transient inward current. In guinea pig cardiac myocytes stimulated at 0.5 Hz and 0.2 Hz, Ca2+ entry through SL Ca2+ channels during a cardiac cycle was approximately 30% and approximately 50%, respectively, of the SR Ca2+ content. In rat myocytes Ca2+ entry via SL Ca2+ channels at 0.5 Hz was approximately 3.5% of the SR Ca2+ content. In the presence of 500 nM thapsigargin Ca2+ entry via SL Ca2+ channels in guinea pig cardiac cells was 39% greater than in controls, suggesting a larger contribution of this mechanism to the Ca2+ transient when the SR is depleted of Ca2+. These results provide quantitative support to the understanding of the relationship between Ca2+ entry and the SR Ca2+ content and may help to explain differences in the Ca2+ handling observed in different species.
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/9138577-1651654,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9138577-1696371,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9138577-2158147,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9138577-2443659,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9138577-2473193,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9138577-2475607,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9138577-2540697,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9138577-2579587,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9138577-2750887,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9138577-364994,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9138577-6275271,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9138577-6346892,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9138577-7357691,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9138577-7473221,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9138577-7473222,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9138577-7614721,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9138577-7697203,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9138577-7864219,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9138577-8046643,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9138577-8067399,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9138577-8120810,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9138577-8275530,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9138577-8368279,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9138577-8488088,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9138577-8755995,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9138577-8772444,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9138577-8785306,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9138577-8799895
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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 |
Mar
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pubmed:issn |
0006-3495
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
72
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1319-26
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:9138577-Action Potentials,
pubmed-meshheading:9138577-Animals,
pubmed-meshheading:9138577-Cadmium,
pubmed-meshheading:9138577-Caffeine,
pubmed-meshheading:9138577-Calcium,
pubmed-meshheading:9138577-Calcium Channels,
pubmed-meshheading:9138577-Cells, Cultured,
pubmed-meshheading:9138577-Electric Conductivity,
pubmed-meshheading:9138577-Guinea Pigs,
pubmed-meshheading:9138577-Heart,
pubmed-meshheading:9138577-Heart Ventricles,
pubmed-meshheading:9138577-Kinetics,
pubmed-meshheading:9138577-Myocardium,
pubmed-meshheading:9138577-Niflumic Acid,
pubmed-meshheading:9138577-Patch-Clamp Techniques,
pubmed-meshheading:9138577-Rats,
pubmed-meshheading:9138577-Sarcoplasmic Reticulum,
pubmed-meshheading:9138577-Thapsigargin,
pubmed-meshheading:9138577-Time Factors
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pubmed:year |
1997
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pubmed:articleTitle |
Measurements of Ca2+ entry and sarcoplasmic reticulum Ca2+ content during the cardiac cycle in guinea pig and rat ventricular myocytes.
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pubmed:affiliation |
Imperial College School of Medicine, National Heart and Lung Institute, London, England. c.terracciano@ic.ac.uk
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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