The magnitude of the noradrenaline-induced contractions of dog middle cerebral arteries was less than that seen in the vertebral, common carotid, femoral and renal arteries. Noradrenaline and clonidine produced a similar magnitude of maximum contractions in the middle cerebral arteries, whereas methoxamine produced no significant contractions in the same arteries. In the extracranial arteries, noradrenaline and methoxamine produced significantly larger contractions than clonidine. Binding studies revealed no specific 3H-prazosin binding sites in the cerebral arteries, though such binding sites were evident in the case of extracranial arteries. 3H-Yohimbine binding studies revealed the presence of two classes of binding sites with high and low affinities in both cerebral and extracranial arteries. After superior cervical ganglionectomy, noradrenaline- and clonidine-induced contractions of the denervated middle cerebral arteries were not altered, compared with the control arteries. A 3H-yohimbine binding study was also performed using the denervated cerebral arteries. This study revealed that there was a low affinity 3H-yohimbine binding site, whereas high affinity 3H-yohimbine binding site was not detectable. These results suggest the presence of two different binding sites with high and low affinity for alpha 2 adrenoceptors, which we are classifying into alpha 2H and alpha 2L subtypes. The high affinity sites, alpha 2H adrenoceptors, are presynaptically located while the low affinity sites, alpha 2L adrenoceptors, located postsynaptically. The noradrenaline-induced contractions are probably mediated by postsynaptic low affinity sites of alpha 2 adrenoceptors (alpha 2L adrenoceptors) in the cerebral arteries and mainly by alpha 1 adrenoceptors in the extracranial arteries.