The effects of hibernation on endothelium-dependent vasodilatation were investigated in the golden hamster carotid artery, paying special attention to hibernating body temperature (10 °C). To record mechanical and electrical membrane responses, we applied pharmacological (organ bath) and electrophysiological (microelectrode) techniques, using acetylcholine (ACh; 0.001-100 µM) and ATP (0.01-1000 µM) for endothelium-dependent vasodilatation and sodium nitroprusside (SNP; 0.05-10 µM) for endothelium-independent vasodilatation. At 34 °C, ACh, ATP and SNP each induced a relaxation or a hyperpolarization, and these responses were similar in all the preparations from control and hibernated animals. At 10 °C, on the other hand, ACh-induced relaxations and hyperpolarizations were reduced to approximately 35 % and 50 % of the euthermic level in controls and 1 % and 4 % of the euthermic level in hibernated animals, respectively. In contrast, at 10 °C, ATP induced only a contraction or depolarization in all preparations with no significant difference between control and hibernated animals. SNP-induced relaxations and hyperpolarizations obtained at 34 °C were not attenuated by cooling to 10 °C. In the presence of a P2X receptor blocker, piridoxal phosphate-6-azophenyl-2â,4â-disulphonic acid (PPADS; 5 µM), at 34 °C ATP-induced relaxations and hyperpolarizations were significantly enhanced whereas no responses were induced by ATP at 10 °C. After endothelium removal, on the other hand, ATP induced only a contraction or depolarization at both 34 °C and 10 °C. These results suggest that depression of endothelium-dependent vasodilator responses to ACh and ATP may occur in the hibernating golden hamster carotid artery.