The present study investigated the bradycardiac responses to brain ischemia for approximately 30s before and after intravenous administration of hexamethonium (C6, 15 mg/kg) in urethane-anesthetized spontaneously breathing rabbits. The brain ischemia was performed by clamping both common carotid arteries in rabbits whose vertebral arteries were previously occluded. The brain ischemia caused bradycardia, pressor response and apnea. Administration of C6 blocked the bradycardia evoked by brain ischemia and reduced pressor response at the initial period after the onset of brain ischemia. The brain ischemia-induced apnea was not significantly altered by C6-treatment. In a separate series of experiments, we examined the effects of C6 on the response of heart rate (HR) to vagal stimulation in rabbits following unilateral vagotomy. Electrical stimulation of the peripheral end of the cut left vagus nerve that selectively activated myelinated fibers caused the bradycardia and this effect was entirely blocked by administration of C6. When the intensity of stimulus to activate both myelinated and non-myelinated fibers was increased, part of the bradycardia was retained following C6 administration. These results suggest that the brain ischemia-induced bradycardia is totally mediated through the activation of myelinated efferent fibers in the vagus nerve.