The possibility that putative transmitters may influence the aortic nerve stimulation-produced bradycardia and depressor responses was examined in urethane- and chloralose-anesthetized, paralyzed and artificially ventilated rabbits. The ipsilateral microinjection of gamma-aminobutyric acid (GABA, 2-4 micrograms) or morphine hydrochloride (2-4 micrograms) into the nucleus tractus solitarii (NTS) area could partially block the evoked bradycardia and depressor responses produced by stimulation of the aortic nerve without influencing the basal blood pressure and heart rate. This blocking effect of either GABA or morphine was dose-related. Pretreatment with GABA receptor antagonist bicuculline methiodide (0.15-0.20 micrograms) and opiate receptor antagonist naloxone hydrochloride (1-2 micrograms) into the same medullary area completely abolished the effect of GABA and morphine, respectively. Application of bicuculline also greatly antagonized the effect of morphine, but the blocking effect of GABA on the evoked bradycardia and depressor responses still existed following the pretreatment of naloxone. These results indicate that GABAergic and opiate systems present at the NTS exert an inhibitory influence on the evoked baroreflexes and inhibitory effect of the latter may be related to the activation of GABAergic receptor in this nucleus.