Blood flow (Q) and O2 uptake (Vo2) were measured in the intact autoperfused left hindlimb (less paw) of anesthetized paralyzed dogs ventilated at constant rate with either room air (normoxia) or 9.1% O2 in N2 (hypoxia) for 20-min periods. One group of 10 dogs was given 3.0 mg/kg phenoxybenzamine (alpha-block) and was subjected to the sequence of normoxia, hypoxia, normoxia. The sequence was repeated after 1.0 mg/kg propranolol (beta-block). A second group of 10 was treated the same but was not given adrenergic blockers (no block). A third group of 10 was made hypoxic only once after the sciatic and femoral nerves to the prepared limb were severed (denervated). Decreased O2 availability during hypoxia limited both total and limb V02 in all cases. Limb Q did not change, but vascular resistance increased in the no-block group with onset of hypoxia and a brisk transient hyperemia occurred with reoxygenation. After both alpha- and beta-block no change occurred in limb resistance with reoxygenation. A similar result was obtained in the denervated limb. These results indicated that the transient hyperemia following hypoxia was the result of altered states of neurally mediated vascular tone, mostly sympathetic, and was not due to local metabolic vasodilation or altered blood levels of catecholamines during a 20-min period of hypoxia.