Target site of inhibition of baroreflex vagal bradycardia by nasal stimulation

Abstract

We have previously reported that stimulation of nasal mucosa inhibits baroreflex vagal bradycardia (BVB) and this inhibition was mediated exclusively by the trigeminal nerve, and occurred principally at pontomedullary level. In this study, to identify the target site of the inhibition, several types of experiments were conducted in chloralose-urethane-anesthetized, beta-adrenergic receptor-blocked rats. Afferent discharges in the ethmoidal nerve (EN5) were increased in response to nasal stimulation by smoke, and electrical stimulation of the EN5 suppressed BVB induced by electrical stimulation of the aortic depressor nerve (ADN). Electrical stimulation of the EN5 inhibited vagal bradycardia evoked by either electrical or chemical stimulation of the nucleus tractus solitarius (NTS), while it rather facilitated bradycardia by stimulation of the nucleus ambiguus (NA) region. Microstimulation of the NTS induced antidromic compound spike potential along the ADN but this was not affected by stimulation of the EN5. ADN-evoked field potentials and unitary responses of neurons in the NTS were suppressed by stimulation of the EN5. These results suggested that barosensitive neurons in the NTS are the major target sites of inhibition of BVB by nasal stimulation in rats.