A GABAergic mechanism in the posterior hypothalamus modulates baroreflex bradycardia.

Several laboratories have shown that electrical stimulation in the posterior hypothalamus inhibits the baroreceptor reflex. However, the results of these studies are difficult to interpret since it is not known if the attenuation of the baroreflex results from activation of axons of passage or from stimulation of hypothalamic cell bodies. The purpose of this study was to determine the effects of chemical stimulation of posterior hypothalamic neurons upon the baroreflex. Arterial baroreceptors were activated by increasing the pressure in an isolated carotid sinus in anesthetized cats and by an increased arterial pressure following intravenous injection of phenylephrine in both anesthetized cats and rats. The baroreceptor reflex was evaluated before and after a GABA antagonist (picrotoxin) was microinjected into the posterior hypothalamus. The bradycardia, but not the depressor response, elicited by increasing carotid sinus pressure was attenuated after unilateral microinjections of picrotoxin into the posterior hypothalamus. In addition, the heart rate response to a phenylephrine-evoked rise in arterial pressure was reduced after picrotoxin was microinjected in both the cats and the rats. Microinjection of a GABA agonist (muscimol) into the same hypothalamic site returned resting heart rate and arterial pressure to levels seen prior to picrotoxin. These results show that the depression of the bradycardia produced by hypothalamic stimulation results from activation of cell bodies in the posterior hypothalamus. This hypothalamic effect upon the baroreflex bradycardia may involve a GABAergic mechanism.