| Effects of targeted deletion of A1 adenosine receptors on postischemic cardiac function and expression of adenosine receptor subtypes. | |
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MedLine Citation:
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PMID: 16679400 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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To examine ischemic tolerance in the absence of A(1) adenosine receptors (A(1)ARs), isolated wild-type (WT) and A(1)AR knockout (A(1)KO) murine hearts underwent global ischemia-reperfusion, and injury was measured in terms of functional recovery and efflux of lactate dehydrogenase (LDH). Hearts were analyzed by real-time RT-PCR both at baseline and at intervals during ischemia-reperfusion to determine whether compensatory expression of other adenosine receptor subtypes occurs with either A(1)AR deletion and/or ischemia-reperfusion. A(1)KO hearts had higher baseline coronary flow (CF) and left ventricular developed pressure (LVDP) than WT hearts, whereas heart rate was unchanged by A(1)AR deletion. After 20 min of ischemia, CF was attenuated in A(1)KO compared with WT hearts, and this reduction persisted throughout reperfusion. Final recovery of LVDP was decreased in A(1)KO hearts (54.4 +/- 5.1 vs. WT 81.1 +/- 3.4% preischemic baseline) and correlated with higher diastolic pressure during reperfusion. Postischemic efflux of LDH was greater in A(1)KO compared with WT hearts. Real-time RT-PCR demonstrated the absence of A(1)AR transcript in A(1)KO hearts, and the message for A(2A), A(2B), and A(3) adenosine receptors was similar in uninstrumented A(1)KO and WT hearts. Ischemia-reperfusion increased A(2B) mRNA expression 2.5-fold in both WT and A(1)KO hearts without changing A(1) or A(3) expression. In WT hearts, ischemia transiently doubled A(2A) mRNA, which returned to preischemic level upon reperfusion, a pattern not observed in A(1)KO hearts. Together, these data affirm the cardioprotective role of A(1)ARs and suggest that induced expression of other adenosine receptor subtypes may participate in the response to ischemia-reperfusion in isolated murine hearts. |
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Authors:
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R Ray Morrison; Bunyen Teng; Peter J Oldenburg; Laxmansa C Katwa; Jurgen B Schnermann; S Jamal Mustafa |
Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural Date: 2006-05-05 |
Journal Detail:
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Title: American journal of physiology. Heart and circulatory physiology Volume: 291 ISSN: 0363-6135 ISO Abbreviation: Am. J. Physiol. Heart Circ. Physiol. Publication Date: 2006 Oct |
Date Detail:
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Created Date: 2006-09-15 Completed Date: 2006-11-09 Revised Date: 2007-11-14 |
Medline Journal Info:
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Nlm Unique ID: 100901228 Medline TA: Am J Physiol Heart Circ Physiol Country: United States |
Other Details:
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Languages: eng Pagination: H1875-82 Citation Subset: IM |
Affiliation:
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Division of Critical Care Medicine, St. Jude Children's Research Hospital, 332 N. Lauderdale St., MS 734, Memphis, TN 38105, USA. ray.morrison@stjude.org |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Coronary Vessels / physiology Female Gene Deletion Gene Expression Regulation / physiology Lactate Dehydrogenases / metabolism Male Mice Mice, Knockout Myocardial Contraction / physiology Myocardial Ischemia / genetics*, metabolism Myocardium / metabolism* RNA, Messenger / genetics, metabolism Receptor, Adenosine A1 / genetics*, metabolism Receptor, Adenosine A2A / genetics*, metabolism Receptor, Adenosine A2B / genetics*, metabolism Receptor, Adenosine A3 / genetics*, metabolism Regional Blood Flow / physiology Reperfusion Injury / physiopathology* Vasodilation / physiology |
| Grant Support | |
ID/Acronym/Agency:
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HL-074001/HL/NHLBI NIH HHS; HL-27339/HL/NHLBI NIH HHS; HL-60047/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/RNA, Messenger; 0/Receptor, Adenosine A1; 0/Receptor, Adenosine A2A; 0/Receptor, Adenosine A2B; 0/Receptor, Adenosine A3; EC 1.1.-/Lactate Dehydrogenases |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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