This study examined in vitro tyramine (TY)-induced contractions of the isolated ring segments of the rabbit basilar and ear arteries in relation to their sympathetic innervations. The TY dose–response relationship in the basilar artery was not affected by cocaine, chronic sympathectomy, or reser-pine pretreatment. However, these treatments shifted the TY dose-response relationship in the ear arteries significantly to the right. These results indicate that the TY-induced contraction in the basilar artery is due solely to its direct stimulation of the postsynaptic a-receptors, but in the ear artery it is due both to its indirect [release of norepinephrine (NE)] and direct actions. The failure of TY to induce contraction in the basilar artery by the indirect mechanism is probably in part due to a wide synaptic cleft distance and the reported insensitivity of α-receptors of this artery. These results suggest that the endogenous NE releasable from the sympathetic nerve in the basilar artery is insufficient to bring about vasoconstriction. This in turn favors our previous hypothesis that transmural-nerve-stimulation (TNS)-induced constriction of this artery is due to a transmitter other than NE. It further suggests that the functional significance of the sympathetic innervations to different regions of the vessels is highly variable even when they are of the same ganglionic origin.