Fetal responses to acute hypoxemia include bradycardia, increase in blood pressure, and peripheral vasoconstriction. Peripheral vasoconstriction contributes to the redistribution of the cardiac output away from ancillary vascular beds toward myocardial, cerebral, and adrenal circulations. We investigated the effect of alpha-adrenergic receptor blockade on this fetal response. Fluorescent microspheres were used to measure cardiac output distribution during basal and hypoxemic conditions with and without phentolamine treatment. Phentolamine altered basal cardiac output distribution, indicating a basal alpha-adrenergic tone, but this was mainly noted at the earlier stages of incubation. During hypoxemia, phentolamine prevented vasoconstriction in the carcass. At day 19 of incubation, the percent cardiac output distributed to the carcass increased by 20% compared with a decrease in the control group by 17%. Phentolamine markedly attenuated the subsequent redistribution of the cardiac output toward the brain (from +102% in the control group to -25% in the phentolamine-treated group) and the heart (from +196% in the control group to +69% in the phentolamine-treated group). In the chick embryo, alpha-adrenergic mechanisms contribute to the maintenance of basal vascular tone and to the redistribution of the cardiac output away from the peripheral circulations toward the brain and heart during hypoxemic conditions.