Bradycardia was evoked in rabbits anaesthetized with chloralose-urethane by electrical stimulation (200 or 300 microA, 1 ms, 60 s-1 for 9 s, repeated every 5 min) of a selected point in the caudal hypothalamus 1.5 mm from the midline dorsal to the mammillary bodies. Phenoxybenzamine, prazosin and yohimbine solutions were infused intracerebroventricularly at a rate of 20 microliters min-1. Phenoxybenzamine did not cause any effects additional to those attributable to the solvent alone. Prazosin attenuated the evoked bradycardia at all doses (40 to 300 micrograms) and altered resting heart rate (HR) and arterial blood pressure (BP) after the higher doses. Yohimbine (200 + 300 micrograms) attenuated the bradycardia with negligible effects on HR and BP. Prazosin and yohimbine were given intravenously. Both caused dose-related attenuation of evoked bradycardia but prazosin also lowered BP sufficiently for this action alone to account for almost all the loss of bradycardia. The weaker hypotensive action of yohimbine was insufficient to account for the attenuation, a conclusion confirmed in animals whose BP was maintained constant by noradrenaline infusion after cervical spinal transection. In this preparation yohimbine caused dose-related attenuation of the bradycardia. The experiments have shown that yohimbine and probably prazosin also, can prevent hypothalamic stimulation from evoking bradycardia. The results suggest the presence of an alpha-adrenergic pathway from this region of the hypothalamus which projects caudally to increase the gain of the cardio-decelerator baroreceptor reflex in the rabbit.