Characterization of adenosine action in isolated rat renal artery. Possible role of adenosine A(2A) receptors.

Adenosine (0.1-300 microM) induced concentration- and endothelium-dependent relaxation of rat renal artery (RRA). N(G)-Nitro-L-arginine (L-NOARG, 10 microM) significantly reduced adenosine-elicited dilatation, but not the application of indomethacin (10 microM), ouabain (100 microM) or tetraethylammonium (TEA, 500 microM). In the presence of high concentration of K(+) (100 mM) or glibenclamide (1 microM), adenosine-evoked relaxation was almost abolished. 8-(3-Chlorostyril)caffeine (CSC, 0.3-3 microM), 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.