Characterization of adenosine action in isolated rat renal artery -: Possible role of adenosine A2A receptors

Adenosine (0.1-300 muM) induced concentration- and endothelium-dependent relaxation of rat renal artery (RRA). N-G-Nitro-L-arginine (L-NOARG, 10 muM) significantly reduced adenosine-elicited dilatation, but not the application of indomethacin (10 muM), ouabain (100 muM) or tetraethylammonium (TEA, 500 muM). In the presence of high concentration of K+ (100 mM) or glibenclamide (1 muM), adenosine-evoked relaxation was almost abolished. 8-(3-Chlorostyril)caffeine (CSC, 0.3-3 muM), a selective A(2A)-antagonist, significantly reduced adenosine-evoked dilatation in a concentration-dependent manner (pA(2) = 7.29). Conversely, 1,3-dipropyl-8-cyclopentylxanthine (DPCPX, 10 nM), an A(1)-antagonist, did not alter adenosine-induced relaxation. These results indicate that adenosine produces endothelium-dependent relaxation of isolated RRA. Dilatation evoked by adenosine is mediated by predominant releasing of endothelium-derived hiperpolarizing factor (EDHF) and also in one part of nitric oxide (NO) from endothelial cells. The obtained results also suggest that RRA response to adenosine is most likely initiated by activation of endothelial adenosine A(2A) receptors. (C) 2001 Elsevier Science Inc. All rights reserved.