Abstract In cats activation of the dorsal facial area (DFA) in the medulla produced an increase of blood flow in the common carotid artery (CCA). This involves flow increases in both intra-and extra-cranial vessels via cranial parasympathetic nerves. In this study, we attempted to explore transmitter mechanisms involved in vasodilatation in extracranial vascular beds due to DFA activation. Cats were anesthetized with intraperitoneal urethane (350 mg/kg) and chloralose (35 mg/kg). Electrical stimulation (100 μA, 20 Hz, 0.5 ms for 5 s) or microinjection of sodium glutamate (Glu, 0.25 M, 50 nl) in DFA increased the velocity of flow in CCA ipsilateral to the stimulation. After control values were obtained, the animals were subjected to decerebration with transection level just rostral to superior colliculi (precollicular decerebration). The increased CCA flow velocity induced by DFA activation was not altered before and after decerebration. Atropine (muscarinic blocker, 0.5–2.0 mg/kg, i.v.) alone only partially attenuated the increase, but the increase was totally blocked by additional N ω- l-arginine methyl ester (nitric oxide synthase inhibitor) in 7 out of 9 cats. These findings suggest that extracranial vasodilatation induced by DFA activation does not depend on the sympathetic nervous system, but involves the muscarinic- and nitric-oxide-mediated systems.