Isolated rat inferior mesenteric artery response to adenosine: possible participation of Na+/K+-ATPase and potassium channels.

Adenosine (10(-7)-3 x 10(-4) M) produced concentration-dependent and endothelium-independent relaxation of isolated rat inferior mesenteric artery. Application of indomethacin (10(-5) M) or N(G)-nitro-L-arginine (10(-5) M) did did not alter adenosine-elicited relaxation. Conversely, in the presence of high concentration of K+ (100 mM), ouabain (10(-4)) or combination of tetraethylammonium (5 x 10(-4) M) and glibenclamide (10(-6) M), adenosine-evoked relaxant effect was significantly reduced. In K+-free solution, 1-3 mM potassium induced relaxation, which was partially reversed by ouabain (10(-4) M). 1,3-Dipropyl-8-cyclopentylxanthine (10(-9) M), an A1-receptor antagonist, did not affect adenosine-evoked relaxation. Oppositely, 8-(3-chlorostyryl)-caffeine (3 x 10(-7)-10(-6) M), a selective A2A receptor antagonist, significantly inhibited adenosine-induced relaxation in a concentration-dependent manner (pA2 = 6.74). These results indicate that in the isolated rat inferior mesenteric artery, adenosine produces endothelium-independent relaxation, which is partly induced by activation of smooth muscle adenosine A2A receptors, and further mediated by the activation of smooth muscle Na+/K+-ATPase and opening of mixed population of K+ channels.