The cardiovascular effects of the psychotomimetic DOM were investigated in pentobarbital-anesthetized cats. DOM (1,2 and 4 mg/kg, i.v.) produced a rise in mean blood pressure accompanied by bradycardia. DOM (1 and 2 mg/kg, i.v.) also produced a contraction of the decentralized nictitating membrane. The duration of the pressor response to DOM was reduced in magnitude and duration by hexamethonium, by spinal section plus vagotomy, and by carotid sinus denervation plus vagotomy. Ventricular--cisternal perfusion of 20 mug DOM resulted in a slow developing hypertensive response. Methylsergid significantly attenuated the pressor response and the contraction of the nictitating membrane induced by i.v. DOM administration. The pressor response to DOM was not altered by phentolamine, propranolol or atropine and vagotomy. Bradycardia induced by DOM was antagonized by carotid sinus denervation plus vagotomy, hexamethonium, spinal sectioning plus vagotomy, and propranolol. Bradycardia induced by DOM is therefore a result of a reflex response to increased blood pressure. The present data thus indicate that the pressor response to DOM consists of two compents: a direct vascular effect mediated via the stimulation of serotonergic receptors; and a second pressor effect, mediated by the central nervous system.