In helically cut strips of dog cerebral, coronary and mesenteric arteries contracted with prostaglandin F2<sub>α</sub>, adenosine, AMP, ADP, ATP and cyclic AMP produced dose-related, persistent relaxation. On the basis of ED<sub>50</sub>s, the relaxant effect seen in cerebral arteries was in the order of AMP, ADP, ATP > adenosine, cyclic AMP > adenine, dibutyryl cyclic AMP > inosine. On the basis of maximum relaxations, the effect was in the order of adenine, dibutyryl cyclic AMP ≧ adenosine, AMP, ADP, ATP > cyclic AMP, inosine. The relaxant responses to adenosine, AMP, ADP, ATP and cyclic AMP were attenuated by treatment with aminophylline, whereas the relaxations induced by dibutyryl cyclic AMP, adenine and inosine were not altered. It is concluded that adenosine, AMP, ADP and ATP, but not adenine and inosine, appear to share receptors underlying arterial relaxations, and the cyclic AMP-induced relaxation does not derive from increments in cellular cyclic AMP. Treatment with aspirin did not alter the relaxant effect of ADP, adenosine and adenine, suggesting that the release of vasoactive prostaglandins is not involved.