Simultaneous measurements of ventral aortic pressure, dorsal aortic pressure, cardiac output, and branchial venous flow were made to assess the effects of external hypoxia on the branchial vasculature in vivo. In addition, the effects of exogenously added amines (epinephrine and serotonin) and their antagonists (prazosin, sotalol, and methysergide) were assessed. The net effect of hypoxia was to increase branchial venous flow. Mechanisms involved in the branchial vasomotor control include an alpha-adrenoceptor-mediated vasoconstriction, as well as a nonadrenergic, possibly serotonergic, vasodilation of the arteriovenous pathway. The arterioarterial vascular resistance remained largely constant during hypoxia: a beta-adrenoceptor vasodilator effect was offset by vasoconstrictor factors that could be unmasked by sotalol treatment. One of these arterioarterial vasoconstrictors may be serotonin (released from serotonergic nerves or neuroepithelial cells), acting on the efferent filamental artery sphincters. The vascular adjustments during hypoxia increased the portion of cardiac output that flowed to the arteriovenous pathway. This may be of importance in providing the heart and the ion-regulatory cells of the filamental epithelium with oxygenated blood.