ATP produces vasodilation via P1 purinoceptors and vasoconstriction via P2 purinoceptors in the isolated rabbit central ear artery.

P1 and P2 purinoceptors mediating mechanical responses in isolated rabbit ear artery were studied by comparing responses to adenosine triphosphate (ATP), alpha, beta-methylene ATP, and adenosine, both when endothelial cells were intact and when they had been removed by mechanical rubbing (as confirmed by histochemical staining and near abolition of relaxation to acetylcholine). alpha, beta-Methylene ATP and ATP (but not adenosine or acetylcholine) contracted preparations at resting tone. alpha, beta-Methylene ATP was significantly more potent as a contractile agent than ATP. Neither was significantly affected by removal of the endothelium. Acetylcholine, ATP, and adenosine relaxed arteries whose tone had been raised by 10(-6) M histamine. Removal of the endothelium virtually abolished relaxations to acetylcholine and significantly decreased those to adenosine and ATP. All relaxations to adenosine and ATP were significantly antagonised by 8-phenyltheophylline, a potent P1 purinoceptor antagonist. alpha, beta-Methylene ATP further contracted the high-tone preparation and was again unaffected by removal of the endothelium. These results confirm that endothelial cells can mediate vasodilation. They also show that adenosine (and ATP) can elicit vasodilation via P1 purinoceptors both on the endothelial cells and on the smooth muscle of the isolated rabbit central ear artery. P2 purinoceptors, however, appear to be located on the smooth muscle only and mediate vasoconstriction.