Preterm infants are often treated with intravenous dopamine to increase mean arterial blood pressure (MAP). However, there are few data regarding cerebrovascular responses of developing animals to dopamine infusions. We studied eight near-term and eight preterm chronically catheterized unanesthetized fetal sheep. We measured cerebral blood flow and calculated cerebral vascular resistance (CVR) at baseline and during dopamine infusion at 2.5, 7.5, 25, and 75 µg · kg¹ · min¹. In preterm fetuses, MAP increased only at 75 µg · kg¹ · min¹ (25 ± 5%), whereas in near-term fetuses MAP increased at 25 µg · kg¹ · min¹ (28 ± 4%) and further at 75 µg · kg¹ · min¹ (51 ± 3%). Dopamine infusion was associated with cerebral vasoconstriction in both groups. At 25 µg · kg¹ · min¹, CVR increased 77 ± 51% in preterm fetuses and 41 ± 11% in near-term fetuses, and at 75 µg · kg¹ · min¹, CVR increased 80 ± 33% in preterm fetuses and 83 ± 21% in near-term fetuses. We tested these responses to dopamine in 11 additional near-term fetuses under -adrenergic blockade (phenoxybenzamine, n = 5) and under dopaminergic D₁-receptor blockade (SCH-23390, n = 6). Phenoxybenzamine completely blocked dopamine's pressor and cerebral vasoconstrictive effects, while D₁-receptor blockade had no effect. Therefore, in unanesthetized developing fetuses, dopamine infusion is associated with cerebral vasoconstriction, which is likely an autoregulatory, -adrenergic response to an increase in blood pressure.