Albino rabbits were anesthetized and artificially ventilated. In two groups of animals the facial nerve on one side was sectioned and/or electrically stimulated at the internal acoustic pore. Hemorrhagic hypotension was induced to reveal a possible parasympathetic vasodilator mechanism, normally masked. The labelled microsphere method was used for flow determination. Section of the facial nerve did not produce any difference between sectioned and intact side, concerning cerebral, ocular and mandibular gland blood flows at normal or low blood pressures. Stimulation of the facial nerve at arterial hypotension produced significant ipsilateral increases in the choroidal and the mandibular gland blood flows. Regional and total cerebral blood flow remained unaffected. The results indicate no or only minimal contribution of the facial nerve to the cerebral vascular tone under conditions of general anesthesia. Further evidence is given in this study for a vasodilator pathway to the eye via the facial nerve, but the resting vasodilator tone under general anesthesia seems to be very low at normotensive as well as hypotensive states.