Reversible impairment of endothelium-dependent relaxation in golden hamster carotid arteries during hibernation.

The effects of hibernation on endothelium-dependent vasodilatation were investigated in the golden hamster carotid artery, paying special attention to hibernating body temperature (10 degrees C). To record mechanical and electrical membrane responses, we applied pharmacological (organ bath) and electrophysiological (microelectrode) techniques, using acetylcholine (ACh; 0.001-100 microM) and ATP (0.01-1000 microM) for endothelium-dependent vasodilatation and sodium nitroprusside (SNP; 0.05-10 microM) for endothelium-independent vasodilatation. At 34 degrees 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 degrees 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 degrees 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 degrees C were not attenuated by cooling to 10 degrees C. In the presence of a P2X receptor blocker, pyridoxal phosphate-6-azophenyl-2',4'-disulphonic acid (PPADS; 5 microM), at 34 degrees C ATP-induced relaxations and hyperpolarizations were significantly enhanced whereas no responses were induced by ATP at 10 degrees C. After endothelium removal, on the other hand, ATP induced only a contraction or depolarization at both 34 degrees C and 10 degrees C. These results suggest that depression of endothelium-dependent vasodilator responses to ACh and ATP may occur in the hibernating golden hamster carotid artery.