Somatosensory and hypothalamic inhibitions of baroreflex vagal bradycardia in rats.

Somatosensory and forebrain mechanisms inhibiting arterial baroreflexes were investigated in chloralose-urethane anesthetized and artificially ventilated rats. Electrical stimulation of the sciatic nerve (ScN) and the hypothalamic pressor area (HP) suppressed baroreflex vagal bradycardia (BVB) and hypotension provoked by electrical stimulation of the aortic depressor nerve (ADN). Suppression of BVB was more marked, but inhibitory potencies of ScN and HP were not different. These two inhibitions were considered to have a functional implication in common, since both were accompanied by increase in hindlimb vascular conductance. A variety of experiments were conducted to localize the target site of ScN and HP inhibitions of BVB. Either ScN or HP stimulations was without effect on antidromic compound spike potentials along ADN evoked by microstimulation of the nucleus tractus solitarius (NTS), precluding the possibility of these inhibitions being presynaptic. Both ScN and HP stimulation suppressed ADN-induced field potentials in the NA region which provoked vagal bradycardia upon microstimulation, but failed to affect ADN-induced responses, either field or unitary, in the NTS region. Antidromic unitary responses in the NA region to vagus cardiac branch stimulation were suppressed by ScN and HP stimulations in NTS-lesioned rats. Intracisternal bicuculline, a GABA antagonist, was found to abolish both ScN and HP inhibitions of BVB, while intracisternal muscimol, a GABA agonist, eliminated bradycardia. These findings suggest that somatosensory and forebrain inhibition of BVB occur principally at the preganglionic cell level and are probably mediated by a GABAergic mechanism.