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DC Field | Value | Language |
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dc.creator | Teng B | - |
dc.creator | Mustafa SJ | - |
dc.date | 2011 | - |
dc.date.accessioned | 2013-05-30T13:00:26Z | - |
dc.date.available | 2013-05-30T13:00:26Z | - |
dc.date.issued | 2013-05-30 | - |
dc.identifier | http://www.dovepress.com/a2a-adenosine-receptor-mediated-increase-in-coronary-flow-in-hyperlipi-a7925 | - |
dc.identifier | http://www.doaj.org/doaj?func=openurl&genre=article&issn=11791454&date=2011&volume=2011&issue=default&spage=59 | - |
dc.identifier.uri | http://koha.mediu.edu.my:8181/jspui/handle/123456789/5542 | - |
dc.description | Bunyen Teng, S Jamal MustafaDepartment of Physiology and Pharmacology and Center for Cardiovascular and Respiratory Sciences, West Virginia University, Morgantown, WV, USAAbstract: Adenosine-induced coronary vasodilation is predominantly A2A adenosine receptor (AR)-mediated, whereas A1 AR is known to negatively modulate the coronary flow (CF). However, the coronary responses to adenosine in hyperlipidemia and atherosclerosis are not well understood. Using hyperlipidemic/atherosclerotic apolipoprotein E (APOE)–knockout mice, CF responses to nonspecific adenosine agonist (5'-N-ethylcarboxamide adenosine, NECA) and specific adenosine agonists (2-chloro-N6-cyclopentyl-adenosine [CCPA, A1 AR-specific] and CGS-21680, A2A AR-specific) were assessed using isolated Langendorff hearts. Western blot analysis was performed in the aorta from APOE and their wild-type (WT) control (C57BL/6J). Baseline CF (expressed as mL/min/g heart weight) was not different among WT (13.23 ± 3.58), APOE (13.22 ± 2.78), and APOE on high-fat diet (HFD) for 12 weeks (APOE-HFD, 12.37 ± 4.76). Concentration response curves induced by CGS-21680 were significantly shifted to the left in APOE and APOE-HFD when compared with WT. CCPA induced an increase in CF only at 10-6 M in all groups and the effect was reversed by the addition of a selective A2A AR antagonist, SCH-58261 (10-6 M), and a significant decrease in CF from baseline was observed. Western blot analysis showed a significant upregulation of A2A AR in the aorta from APOE and APOE-HFD. This study provides the first evidence that CF responses to A2A AR stimulation were upregulated in hyperlipidemic/atherosclerotic animals. The speculation is that the use of A2A AR-specific agonist for myocardial perfusion imaging (such as regadenoson) could overestimate the coronary reserve in coronary artery disease patients.Keywords: hyperlipidemia, atherosclerosis, apolipoprotein E–knockout mice, coronary flow regulation, A2A adenosine receptor | - |
dc.language | eng | - |
dc.publisher | Dove Press | - |
dc.source | Journal of Experimental Pharmacology | - |
dc.title | A2A adenosine receptor-mediated increase in coronary flow in hyperlipidemic APOE–knockout mice | - |
Appears in Collections: | Health Sciences |
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