Cerebral arteries are relatively unresponsive to sympathetic nerve stimulation, in spite of extensive adrenergic innervation. To determine whether these nerves are functional, release of endogenous norepinephrine (NE) was measured using a radioenzymatic assay. Fractional release of NE per stimulation pulse was more than 5 times greater from the rabbit basilar artery than from the ear artery. Thus, while the NE content of the two vessels is quite similar, transmitter release is considerably greater in the basilar artery. Since NE accumulation is also much greater in the basilar artery, it seems possible that an active parameter such as NE release or accumulation may be a better index of functional nerve capacity than NE content. Previous studies have shown that alpha adrenergic blocking agents do not block the contractile response to nerve stimulation of the basilar artery, but actually increase it. Thus, the possibility that blockade of presynaptic adrenergic receptors leads to increased transmitter release was tested. Indeed, both phenoxybenzamine and phentolamine significantly increased stimulation-evoked NE release. It appears that postsynaptic events in cerebral arteries are atypical, while release of transmitter, including modulation by presynaptic alpha adrenergic receptors is similar to other blood vessels.