ArticleAmerican journal of physiology. Heart and circulatory physiology2010
Both A2a and A2b adenosine receptors at reperfusion are necessary to reduce infarct size in mouse hearts.
Article in American journal of physiology. Heart and circulatory physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 53 citations in OpenAlex.
- Nanoparticle-Based Targeted Drug Delivery Methods for Heart-Specific Distribution in Cardiovascular Therapy.Pharmaceutics · 2025Review
- Review
- Remote Conditioning by Rhythmic Compression of Limbs Ameliorated Myocardial Infarction by Downregulation of InflammationFrontiers in cardiovascular medicine · 2021Article
- Electroacupuncture improves myocardial ischemia injury via activation of adenosine receptors.Purinergic signalling · 2020Article
- Ticagrelor Prevents Endothelial Cell Apoptosis through the Adenosine Signalling Pathway in the Early Stages of Hypoxia.Biomolecules · 2020Article
- Role of Cardiac AFrontiers in pharmacology · 2020Review
- Novel Therapeutic Targets for Hypoxia-Related Cardiovascular Diseases: The Role of HIF-1.Frontiers in physiology · 2020Review
- Plasma levels of the cardiovascular protective endogenous nucleoside adenosine are reduced in patients with primary aldosteronism without affecting ischaemia-reperfusion injury: A prospective case-control study.European journal of clinical investigation · 2019Article
- Article
- Inhibition of tPA-induced hemorrhagic transformation involves adenosine A2b receptor activation after cerebral ischemia.Neurobiology of disease · 2017Article
- Cardioprotective Effect of the SDF-1α/CXCR4 Axis in Ischemic Postconditioning in Isolated Rat Hearts.Korean circulation journal · 2017Article
- Signalling pathways and mechanisms of protection in pre- and postconditioning: historical perspective and lessons for the future.British journal of pharmacology · 2015Review
- Extracellular signalling molecules in the ischaemic/reperfused heart - druggable and translatable for cardioprotection?British journal of pharmacology · 2015Review
- Cardiac purinergic signalling in health and disease.Purinergic signalling · 2015Review
- Extracellular Adenosine Formation by Ecto-5'-Nucleotidase (CD73) Is No Essential Trigger for Early Phase Ischemic Preconditioning.PloS one · 2015Article
- Adenosine 2B Receptor Activation Reduces Myocardial Reperfusion Injury by Promoting Anti-Inflammatory Macrophages Differentiation via PI3K/Akt Pathway.Oxidative medicine and cellular longevity · 2015Article
- PET/MRI assessment of the infarcted mouse heart.Nuclear instruments & methods in physics research. Section A, Accelerators, spectrometers, detectors and associated equipment · 2014Article
- MRI and PET in mouse models of myocardial infarction.Journal of visualized experiments : JoVE · 2013Article
- Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I.Nature medicine · 2013Article
- The CD39-adenosinergic axis in the pathogenesis of renal ischemia-reperfusion injury.Purinergic signalling · 2013Review
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Authors and funding
5 authors at 3 institutions in 3 countries.
Funding
Abstract
Pre- and postconditioning depend on the activation of adenosine receptors (ARs) at the end of the index ischemia. The aim of this study was to determine which receptor subtypes must be activated. In situ mouse hearts underwent 30 min of regional ischemia, followed by 2 h of reperfusion. As expected, either ischemic postconditioning (6 cycles of 10 s of reperfusion and 10 s of coronary occlusion) or infusion of the selective A(2b) adenosine receptor (A(2b)AR) agonist BAY60-6583 (BAY60) for 60 min, starting 5 min before reperfusion reduced infarct size in wild-type C57Bl/6N mice. Protection from either was abolished by the selective A(2b)AR antagonist MRS-1754, confirming a role for A(2b)AR. Additionally, the coadministration of ischemic postconditioning and a selective A(2a)AR antagonist led to the loss of protection as well. 5'-Ectonucleotidase (CD73) is thought to be necessary for the production of adenosine during ischemia. As predicted, ischemic postconditioning did not protect CD73 knockout mice. Selective agonists of either A(2b)AR (BAY60) or A(2a)AR (CGS-21680), as well as the coadministration of ischemic postconditioning and BAY60, also failed to protect hearts of the CD73 knockout mice. But the nonselective A(1)/A(2)AR agonist 5'-(N-ethylcarboxamido)adenosine (NECA) was protective, suggesting that the activation of multiple AR subtypes might be required. The coadministration of CGS-21680 and BAY60 also elicited profound protection, indicating that two AR subtypes, A(2a) and A(2b), must be simultaneously activated for protection to occur.
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