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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
5
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pubmed:dateCreated |
1997-3-3
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pubmed:abstractText |
The mechanism by which chloride increases sarcoplasmic reticulum (SR) Ca2+ permeability was investigated. In the presence of 3 microM Ca2+, Ca2+ release from 45Ca(2+)-loaded SR vesicles prepared from procine skeletal muscle was increased approximately 4-fold when the media contained 150 mM chloride versus 150 mM propionate, whereas in the presence of 30 nM Ca2+, Ca2+ release was similar in the chloride- and the propionate-containing media. Ca(2+)-activated [3H]ryanodine binding to skeletal muscle SR was also increased (2- to 10-fold) in media in which propionate or other organic anions were replaced with chloride; however, chloride had little or no effect on cardiac muscle SR 45Ca2+ release or [3H]ryanodine binding. Ca(2+)-activated [3H]ryanodine binding was increased approximately 4.5-fold after reconstitution of skeletal muscle RYR protein into liposomes, and [3H]ryanodine binding to reconstituted RYR protein was similar in chloride- and propionate-containing media, suggesting that the sensitivity of the RYR protein to changes in the anionic composition of the media may be diminished upon reconstitution. Together, our results demonstrate a close correlation between chloride-dependent increases in SR Ca2+ permeability and increased Ca2+ activation of skeletal muscle RYR channels. We postulate that media containing supraphysiological concentrations of chloride or other inorganic anions may enhance skeletal muscle RYR activity by favoring a conformational state of the channel that exhibits increased activation by Ca2+ in comparison to the Ca2+ activation exhibited by this channel in native membranes in the presence of physiological chloride (< or = 10 mM). Transitions to this putative Ca(2+)-activatable state may thus provide a mechanism for controlling the activation of RYR channels in skeletal muscle.
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pubmed:grant |
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/8913591-1011246,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8913591-1334225,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8913591-1418241,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8913591-1554713,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8913591-1621949,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8913591-1692609,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8913591-2057528,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8913591-2443015,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8913591-3001218,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8913591-3284380,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8913591-4056734,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8913591-4519607,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8913591-6259360,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8913591-7532019,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8913591-7548007,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8913591-7679249,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8913591-7742348,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8913591-7852382,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8913591-7948689,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8913591-8001396,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8913591-8010748,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8913591-8023884,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8913591-8023902,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8913591-8075313,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8913591-8075325,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8913591-8094902,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8913591-8229822,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8913591-8245817,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8913591-8245818,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8913591-8276794,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8913591-8384784
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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 |
Nov
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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 |
71
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
2522-30
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:8913591-Animals,
pubmed-meshheading:8913591-Calcium,
pubmed-meshheading:8913591-Calcium Channels,
pubmed-meshheading:8913591-Cell Compartmentation,
pubmed-meshheading:8913591-Cell-Free System,
pubmed-meshheading:8913591-Chlorides,
pubmed-meshheading:8913591-Heart,
pubmed-meshheading:8913591-Liposomes,
pubmed-meshheading:8913591-Muscle, Skeletal,
pubmed-meshheading:8913591-Muscle Proteins,
pubmed-meshheading:8913591-Myocardium,
pubmed-meshheading:8913591-Nitrates,
pubmed-meshheading:8913591-Perchloric Acid,
pubmed-meshheading:8913591-Ryanodine,
pubmed-meshheading:8913591-Ryanodine Receptor Calcium Release Channel,
pubmed-meshheading:8913591-Sarcoplasmic Reticulum,
pubmed-meshheading:8913591-Swine
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pubmed:year |
1996
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pubmed:articleTitle |
Chloride-dependent sarcoplasmic reticulum Ca2+ release correlates with increased Ca2+ activation of ryanodine receptors.
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pubmed:affiliation |
Department of Veterinary PathoBiology, University of Minnesota, St. Paul 55108, USA. fruen001@maroon.tc.umn.edu
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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