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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Adenosine induces C1- efflux in endothelial cells via a pertussis toxin-sensitive G protein.

To examine the biological role of adenosine A1 receptors in bovine pulmonary artery endothelial cells, we measured intracellular Cl-concentration [Cl-]i, using 10mM 6-methoxy-N-(3-sulfopropyl) quinolinium monohydrate (SPQ). N6-cyclopentyladenosine (CPA), a selective A1 agonist, at 10(-8)M to 10(-5)M, rapidly decreased [Cl-]i by 30% to 51%, without a rapid elevation in [Ca2+]i and cyclic AMP. This reduction in [Cl-]i was completely inhibited by 10(-8)M FK453 (a selective A1 antagonist), 500ng/ml pertussis toxin ( IAP), and 2.5mM N-phenylanthranilic acid (NPA) (a Cl- channel blocker). We conclude that an A1 receptor in endothelial cells activates Cl- efflux via a PTX-sensitive G protein.[1]

References

  1. Adenosine induces C1- efflux in endothelial cells via a pertussis toxin-sensitive G protein. Arima, M., Ueda, S., Matsushita, S., Ozawa, T., Yamaguchi, H. Biochem. Biophys. Res. Commun. (1994) [Pubmed]
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