Potentiation of a cardioinhibitory reflex by hypothalamic stimulation in the rabbit.

Repetitive stimulation of an area within the lateral hypothalamus, near the mammillothalamic tract, evoked pressor responses with bradycardia in anaesthetized rabbits. With weak stimulation (cathodal pulses below 75--150 microamperemeter, 1 msec duration, 60--100 per sec for 5--9 sec) the pressor responses were accompanied by bradycardia similar in intensity to that evoked by i.v. administration of noradrenaline. Stronger stimulating currents evoked an intense bradycardia that could not have arisen solely through the baroreceptor reflex. With these stronger currents the heart rate sometimes fell, transiently, to less than 20% of the resting rate. After denervation of the 4 main buffer nerves (sinus and aortic nerves), hypothalamic stimulation could not readily evoke bradycardia, although the pressor, respiratory and other effects remained. When the baroreceptor afferents were activated, either by evoked pressor responses in rabbits whose buffer nerves were intact or by electrical stimulation of the central ends of divided aortic nerves, strong hypothalamic stimulation augmented the bradycardia evoked reflexly from these baroreceptor afferents. This evidence suggests that electrical stimulation of this area in the hypothalamus may facilitate the cardioinhibitory component of the baroreceptor reflex in the rabbit.