| In situ SR function in postinfarction myocytes. | |
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MedLine Citation:
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PMID: 10601161 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Previous studies have shown lower systolic intracellular Ca(2+) concentrations ([Ca(2+)](i)) and reduced sarcoplasmic reticulum (SR)-releasable Ca(2+) contents in myocytes isolated from rat hearts 3 wk after moderate myocardial infarction (MI). Ca(2+) entry via L-type Ca(2+) channels was normal, but that via reverse Na(+)/Ca(2+) exchange was depressed in 3-wk MI myocytes. To elucidate mechanisms of reduced SR Ca(2+) contents in MI myocytes, we measured SR Ca(2+) uptake and SR Ca(2+) leak in situ, i.e., in intact cardiac myocytes. For sham and MI myocytes, we first demonstrated that caffeine application to release SR Ca(2+) and inhibit SR Ca(2+) uptake resulted in a 10-fold prolongation of half-time (t(1/2)) of [Ca(2+)](i) transient decline compared with that measured during a normal twitch. These observations indicate that early decline of the [Ca(2+)](i) transient during a twitch in rat myocytes was primarily mediated by SR Ca(2+)-ATPase and that the t(1/2) of [Ca(2+)](i) decline is a measure of SR Ca(2+) uptake in situ. At 5.0 mM extracellular Ca(2+), systolic [Ca(2+)](i) was significantly (P </= 0.05) lower (337 +/- 11 and 416 +/- 18 nM in MI and sham, respectively) and t(1/2) of [Ca(2+)](i) decline was significantly longer (0.306 +/- 0.014 and 0.258 +/- 0.014 s in MI and sham, respectively) in MI myocytes. The 19% prolongation of t(1/2) of [Ca(2+) ](i) decline was associated with a 23% reduction in SR Ca(2+)-ATPase expression (detected by immunoblotting) in MI myocytes. SR Ca(2+) leak was measured by a novel electrophysiological technique that did not require assigning empirical constants for intracellular Ca(2+) buffering. SR Ca(2+) leak rate was not different between sham and MI myocytes: the time constants of SR Ca(2+) loss after thapsigargin were 290 and 268 s, respectively. We conclude that, independent of decreased SR filling by Ca(2+) influx, the lower SR Ca(2+) content in MI myocytes was due to reduced SR Ca(2+) uptake and SR Ca(2+)-ATPase expression, but not to enhanced SR Ca(2+) leak. |
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Authors:
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X Q Zhang; Y C Ng; R L Moore; T I Musch; J Y Cheung |
Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S. |
Journal Detail:
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Title: Journal of applied physiology (Bethesda, Md. : 1985) Volume: 87 ISSN: 8750-7587 ISO Abbreviation: J. Appl. Physiol. Publication Date: 1999 Dec |
Date Detail:
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Created Date: 2000-02-03 Completed Date: 2000-02-03 Revised Date: 2007-11-14 |
Medline Journal Info:
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Nlm Unique ID: 8502536 Medline TA: J Appl Physiol Country: UNITED STATES |
Other Details:
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Languages: eng Pagination: 2143-50 Citation Subset: IM |
Affiliation:
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Department of Medicine, Milton S. Hershey Medical Center, Pennsylvania State University, Hershey, Pennsylvania 17033, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Caffeine / pharmacology Calcium / metabolism, pharmacokinetics Calcium-Transporting ATPases / metabolism Cell Membrane Permeability Heart / physiopathology* Intracellular Membranes / metabolism Male Myocardial Infarction / metabolism, pathology, physiopathology* Myocardium / cytology, metabolism Rats Rats, Sprague-Dawley Sarcoplasmic Reticulum / enzymology, metabolism, physiology* |
| Grant Support | |
ID/Acronym/Agency:
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DK46678/DK/NIDDK NIH HHS; HL40306/HL/NHLBI NIH HHS; HL58672/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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58-08-2/Caffeine; 7440-70-2/Calcium; EC 3.6.1.8/Calcium-Transporting ATPases |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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