ArticleArteriosclerosis, thrombosis, and vascular biology2013
Ecto-5'-nucleotidase, CD73, is an endothelium-derived hyperpolarizing factor synthase.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 36 citations in OpenAlex.
- NADInternational journal of molecular sciences · 2026Article
- Extracellular Purine Metabolism-Potential Target in Multiple Sclerosis.Molecular neurobiology · 2024Review
- Identification of CD73 as the Antigen of an Antigen-Unknown Monoclonal Antibody Established by Exosome Immunization, and Its Antibody-Drug Conjugate Exerts an Antitumor Effect on Glioblastoma Cell Lines.Pharmaceuticals (Basel, Switzerland) · 2022Article
- Appraisal of novel azomethine-thioxoimidazolidinone conjugates as ecto-5'-nucleotidase inhibitors: synthesis and molecular docking studies.RSC advances · 2022Article
- Impact of impaired cerebral blood flow autoregulation on cognitive impairment.Frontiers in aging · 2022Review
- Coronary Microvascular Dysfunction and Heart Failure with Preserved Ejection Fraction - implications for Chronic Inflammatory Mechanisms.Current cardiology reviews · 2022Review
- Adenosine kinase inhibition enhances microvascular dilator function and improves left ventricle diastolic dysfunction.Microcirculation (New York, N.Y. : 1994) · 2020Article
- Cell type- and tissue-specific functions of ecto-5'-nucleotidase (CD73).American journal of physiology. Cell physiology · 2019Review
- Impaired L-arginine metabolism marks endothelial dysfunction in CD73-deficient mice.Molecular and cellular biochemistry · 2019Article
- Adenosine Kinase Inhibition Augments Conducted Vasodilation and Prevents Left Ventricle Diastolic Dysfunction in Heart Failure With Preserved Ejection Fraction.Circulation. Heart failure · 2019Article
- Update on the role of endothelial cells in trauma.European journal of trauma and emergency surgery : official publication of the European Trauma Society · 2018Review
- Functional changes in vascular reactivity to adenosine receptor activation in type I diabetic mice.European journal of pharmacology · 2018Article
- The Impact of Purinergic System Enzymes on Noncommunicable, Neurological, and Degenerative Diseases.Journal of immunology research · 2018Review
- Regulation of Coronary Blood Flow.Comprehensive Physiology · 2017Review
- Mesenchymal Stem Cells Induce Expression of CD73 in Human MonocytesFrontiers in immunology · 2017Article
- The Role of Adenosine ABioMed research international · 2017Review
- Role of Adenosine Receptor(s) in the Control of Vascular Tone in the Mouse Pudendal Artery.The Journal of pharmacology and experimental therapeutics · 2016Article
- Role of 2',3'-cyclic nucleotide 3'-phosphodiesterase in the renal 2',3'-cAMP-adenosine pathway.American journal of physiology. Renal physiology · 2014Article
- Endothelial function is impaired in conduit arteries of pannexin1 knockout mice.Biology direct · 2014Article
- Endothelial control of vasodilation: integration of myoendothelial microdomain signalling and modulation by epoxyeicosatrienoic acids.Pflugers Archiv : European journal of physiology · 2014Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
objectiveAdenosine dilates human coronary arteries by activating potassium channels in an endothelial cell-independent manner. Cell surface ecto-5'-nucleotidase (CD73) rapidly dephosphorylates extracellular adenosine 5'-monophosphate to adenosine. We tested the hypothesis that coronary vasodilation to adenine nucleotides is mediated by an endothelial CD73-dependent, extracellular production of adenosine that acts as an endothelium-derived hyperpolarizing factor. METHODS AND
resultsVideomicroscopy showed that adenine nucleotides, but not inosine, potently dilated and hyperpolarized human coronary arteries independent of nitric oxide, prostacyclin, and classical endothelium-derived hyperpolarizing factors, whereas endothelial denudation, adenosine receptor antagonism, adenosine deaminase, or CD73 blockers reduced vasodilations. Liquid chromatography-electrospray ionization-mass spectrometry revealed adenosine accumulation in perfusates from arteries in the presence of adenosine 5'-diphosphate. CD73 was localized on the cell surface of endothelial cells, but not of vascular smooth muscle cells, and its deficiency suppressed vasodilation of mouse coronary arteries to adenine nucleotides and augmented vasodilation to adenosine. Adenosine dose-dependently dilated and hyperpolarized human coronary arteries to a similar extent as adenosine 5'-diphosphate.
conclusionsCoronary vasodilation to adenine nucleotides is associated with endothelial CD73-dependent production of extracellular adenosine that acts as an endothelium-derived hyperpolarizing factor by relaxing and hyperpolarizing underlying vascular smooth muscle cells via activating adenosine receptors. Thus, CD73 is a novel endothelium-derived hyperpolarizing factor synthase in human and mouse coronary arteries.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.