Electrical stimulation (1--50 Hz, 100--500 muA, 0.3 msec pulse duration) of the dorsal or median raphe nucleus in anesthetized rats produces a transient increase in arterial blood pressure. Heart rate and respiratory rate do not appear to change systematically after stimulation. Transections rostral or caudal to the raphe nuclei or electrolytic lesions in the area of the nucleus linearis, pars caudalis abolishes the pressor response to stimulation. Depletion of brain serotonin with p-chlorophenylalanine significantly attenuates the pressor effect of both dorsal and median raphe stimulation. The p-chlorophenylalanine effect can be partially reversed by Ro4-4602, a peripherally acting decarboxylase inhibitor, plus 5-hydroxytryptophan. Fluoxetine, a specific serotonin uptake inhibitor, prolongs the duration of the raphe pressor response and slightly increases its magnitude. Injections of 2-bromolysergic acid diethylamide (BOL), a putative serotonin antagonist, into the anterior hypothalamus/preoptic area significantly attenuates the dorsal raphe pressor effect, whereas treatment of rats with the sympathetic postganglionic blocking agent bretylium prevents the stimulation-induced pressor effect. Taken together, these data suggest that stimulation of the ascending serotonergic neuronal system produces a phasic pressor effect which is mediated, at least in part, by synaptic serotonin.