In isolated ear and mesenteric arteries of rabbit, adenosine inhibited nerve-mediated contractions to a similar extent. However, the amplitude of the excitatory junction potentials evoked by perivascular nerve stimulation was increased by adenosine in the ear artery and decreased in the mesenteric artery. Outflows of noradrenaline and its metabolite, 3,4-dihydroxyphenylglycol, evoked by perivascular nerve stimulation were increased and decreased by adenosine in the ear and mesenteric arteries, respectively. Adenosine hyperpolarized the smooth muscle cells, by increasing potassium conductance of the membrane, with no relation to the endothelial cells. The hyperpolarizing action of adenosine was stronger in the ear artery than in the mesenteric artery. The inhibition of the nerve-mediated contraction by adenosine may be mainly due to postjunctional events in the ear artery and prejunctional events in the mesenteric artery.