| Involvement of sarcoplasmic reticulum in changing intracellular calcium due to Na+/K+-ATPase inhibition in cardiomyocytes. | |
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MedLine Citation:
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PMID: 20651818 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Earlier studies have demonstrated that ouabain-induced increase in [Ca2+]i, as a consequence of sarcolemma (SL) Na+/K+-ATPase inhibition, is associated with activation of both the SL Na+/Ca2+ exchanger and SL Ca2+ channels. In view of the importance of sarcoplasmic reticulum (SR) in the regulation of [Ca2+]i, this study examined the role of SR in ouabain-induced increase in [Ca2+]i in both quiescent and KCl-depolarized cardiomyocytes. For this purpose, adult rat cardiomyocytes were loaded with fura-2 and ouabain-induced changes in [Ca2+]i were monitored upon treatment with or without different agents that are known to influence Ca2+ handling by the intracellular organelles. Ouabain not only increased the basal [Ca2+]i and augmented KCl-induced increase in [Ca2+]i but also produced similar effects on the ATP-induced increase in [Ca2+]i. Treatments of cardiomyocytes with caffeine, ryanodine, or cyclopiazonic acid, which affect SR Ca2+ stores, attenuated the ouabain-induced increase in basal Ca2+ as well as augmentation of the KCl response. Both ryanodine and cyclopiazonic acid produced additional effects, when used in combination with a SL Ca2+ channel inhibitor (verapamil), but not with a Na+/Ca2+ exchange inhibitor (KB-R7943). Inhibitors of Ca2+/calmodulin kinase, protein kinase A, and inositol-3-phosphate receptors were also observed to depress the ouabain-induced increase in [Ca2+]i in cardiomyocytes. On the other hand, mitochondrial Ca2+ transport inhibitors did not exert any effect on the ouabain-induced alterations in [Ca2+]i in cardiomyocytes. Furthermore, ouabain did not show any direct effect on the Ca2+ uptake and Ca2+ release activities of SR or mitochondria. These results suggest an indirect involvement of SR Ca2+ stores in the ouabain-induced increase in [Ca2+]i in cardiomyocytes and indicate the participation of both Ca2+-induced Ca2+ release and regulatory mechanisms in this action. |
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Authors:
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Harjot K Saini-Chohan; Ramesh K Goyal; Naranjan S Dhalla |
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Publication Detail:
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Type: In Vitro; Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Canadian journal of physiology and pharmacology Volume: 88 ISSN: 1205-7541 ISO Abbreviation: Can. J. Physiol. Pharmacol. Publication Date: 2010 Jul |
Date Detail:
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Created Date: 2010-07-23 Completed Date: 2010-11-05 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 0372712 Medline TA: Can J Physiol Pharmacol Country: Canada |
Other Details:
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Languages: eng Pagination: 702-15 Citation Subset: IM |
Affiliation:
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Institute of Cardiovascular Sciences, St. Boniface General Hospital Research Centre, University of Manitoba, Winnipeg, MB R2H 2A6, Canada. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Adenosine Triphosphate
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pharmacology Animals Caffeine / pharmacology Calcium / metabolism* Calcium Signaling / drug effects Calcium-Calmodulin-Dependent Protein Kinases / antagonists & inhibitors Cyclic AMP-Dependent Protein Kinases / antagonists & inhibitors Inositol 1,4,5-Trisphosphate Receptors / antagonists & inhibitors Male Mitochondria, Heart / drug effects, metabolism Myocytes, Cardiac / drug effects, metabolism* Ouabain / pharmacology Potassium Chloride / pharmacology Rats Rats, Sprague-Dawley Ryanodine / pharmacology Sarcolemma / drug effects, metabolism Sarcoplasmic Reticulum / drug effects, metabolism* Sodium-Potassium-Exchanging ATPase / antagonists & inhibitors* |
| Grant Support | |
ID/Acronym/Agency:
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//Canadian Institutes of Health Research |
| Chemical | |
Reg. No./Substance:
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0/Inositol 1,4,5-Trisphosphate Receptors; 15662-33-6/Ryanodine; 56-65-5/Adenosine Triphosphate; 58-08-2/Caffeine; 630-60-4/Ouabain; 7440-70-2/Calcium; 7447-40-7/Potassium Chloride; EC 2.7.11.11/Cyclic AMP-Dependent Protein Kinases; EC 2.7.11.17/Calcium-Calmodulin-Dependent Protein Kinases; EC 3.6.3.9/Sodium-Potassium-Exchanging ATPase |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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