Ecto-5′-Nucleotidase, CD73, Is an Endothelium-Derived Hyperpolarizing Factor Synthase
Author(s) -
Masanori Ohta,
Kazuyoshi Toyama,
David D. Gutterman,
William B. Campbell,
Vincent Lemaître,
Ryutaro Teraoka,
Hiroto Miura
Publication year - 2013
Publication title -
arteriosclerosis thrombosis and vascular biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.007
H-Index - 270
eISSN - 1524-4636
pISSN - 1079-5642
DOI - 10.1161/atvbaha.112.300600
Subject(s) - adenosine , vasodilation , purinergic signalling , endothelium derived hyperpolarizing factor , adenosine monophosphate , adenosine deaminase , endothelium , adenosine a1 receptor , medicine , adenine nucleotide , adenosine a3 receptor , chemistry , endocrinology , adenosine receptor , nucleotidase , biology , biochemistry , receptor , nucleotide , potassium channel , charybdotoxin , gene , agonist
Adenosine 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.
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