Time-dependent potentiation of contractile response to norepinephrine in canine isolated cerebral arteries
The time course of contractile responses to α-adrenoceptor agonists was investigated using various arteries isolated from dogs and monkeys. The contractile response to norepinephrine was increased during the time course of the experiment in canine basilar and internal carotid arteries, whereas the response of isolated canine external carotid arteries and monkey internal carotid arteries did not change significantly. Treatment with 10−7 M propranolol, 5 × 10−6 M cocaine plus 10−5 M hydrocortisone, or 5 × 10−5 M acetylsalicylic acid did not significantly affect the time-dependent potentiation of the norepinephrine-induced contraction in canine internal carotid arteries. The time-dependent enhancement in the response to norepinephrine was also observed in the arterial preparations from which the endothelial cells were removed. The contractile response of canine internal carotid arteries to phenylephrine did not alter significantly throughout the experiments. On the other hand, the responses to clonidine and xylazine were markedly enhanced with time. Significant potentiation of the norepinephrine-induced contraction was observed in canine internal carotid arteries treated with 10−8 M prazosin, whereas 10−8 M yohimbine attenuated the time-dependent potentiation. These results suggest that the contractile responses of isolated canine basilar and internal carotid arteries to norepinephrine are potentiated during the course of the experiment, which is likely to be related, in part, to an enhancement in α2-adrenoceptor mediated contraction.Key words: α2-adrenoceptor, dog, cerebral artery, enhancement of contraction, vascular smooth muscle.