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Received for publication April 30, 2007.
Revised August 3, 2007.
Accepted for publication August 3, 2007.
ATP is an important endogenous mediator in the cardiovascular system. It induces endothelium dependent vasodilatation, but the precise receptor pathway activated in this response is currently under debate. We have used classical bioassay techniques, to show that ATP induced vasodilatation in mesenteric vessels is endothelium dependent. Furthermore, ATP induced vasodilatation was inhibited by both suramin and TNP-ATP, consistent with a P2X1, P2X2 or P2X3 mediated event, and was not potentated by ivermectin, indicating that these responses were not P2X4 receptor mediated. ATP did not induce vasodilatation in vessels from P2X1-/- mice confirming an absolute requirement for this receptor. Finally, in pure cell populations of mouse mesenteric artery endothelial cells, we show that P2X1 mRNA is specifically expressed. However, in line with observations in the brain, the P2X1 present in endothelial cells does not appear to be recognised by conventional antibodies. Together, these results show that ATP induced vasodilatation is mediated by P2X1 receptor activation on mesenteric artery endothelial cells. These observations challenge the current view of purine biology and establish a critical role for P2X1 receptors in the ATP vasodilator pathway.
Key words:
Purinergic, Purinergic, Ion channel regulation, Nucleoside/Nucleotide, Func. analysis receptor/ion channel mutants, Knockout
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