In ovine cerebral arteries, adrenergic-mediated vasoconstrictor responses differ significantly with developmental age. We tested the hypothesis that, in part, these differences are a consequence of altered ₂-adrenergic receptor (₂-AR) density and/or affinity. In fetal (~140 days) and adult sheep, we measured ₂-AR density and affinity with the antagonist [³H]idazoxan in main branch cerebral arteries and other vessels. We also quantified contractile responses in middle cerebral artery (MCA) to norepinephrine (NE) or phenylephrine in the presence of the ₂-AR antagonists yohimbine and idazoxan and contractile responses to the ₂-AR agonists clonidine and UK-14304. In fetal and adult cerebral artery homogenates, ₂-AR density was 201 ± 18 and 52 ± 6 fmol/mg protein, respectively (P < 0.01); however, antagonist affinity values did not differ. In fetal, but not adult, MCA, 10⁷ M yohimbine significantly decreased the pD₂ for NE-induced tension in the presence of 3 × 10⁵ M cocaine, 10⁵ M deoxycorticosterone, and 10⁶ M tetrodotoxin. In fetal, but not adult, MCA, UK-14304 induced a significant decrease in pD₂ for the phenylephrine dose-response relation. In addition, stimulation-evoked fractional NE release was significantly greater in fetal than in adult cerebral arteries. In the presence of 10⁶ M idazoxan to block ₂-AR-mediated inhibition of prejunctional NE release, the fractional NE release was significantly increased in both age groups. We conclude that in fetal and adult ovine cerebral arteries, ₂-AR appear to be chiefly prejunctional. Nonetheless, the fetal cerebral arteries appear to have a significant component of postjunctional ₂-AR.