Inhibition of baroreflex vagal bradycardia by nasal stimulation in rats

Nasal stimulation provokes hypertension and bradycardia. We report here tha t such stimulation inhibits baroreflex vagal bradycardia (BVB). In chloralo se- and urethan-anesthetized, beta-adrenergic receptor-blocked rats, the ao rtic depressor nerves were cut and electrically stimulated to induce BVB. N asal application of smoke, warm distilled water, or cold or hot Ringer solu tion suppressed BVB, but application of warm Ringer solution did not. Smoke -induced inhibition was abolished by trigeminal but not olfactory denervati on. Neither suprapontine decerebration nor Ca spinal cord transection affec ted the inhibition. Bradycardia induced by electrical stimulation of the pe ripheral cut end of the cervical vagus nerve (VIB) was suppressed by long-l asting smoke application. Intravenous prazosin, a proposed blocker of preju nctional inhibition of acetylcholine release from the vagus terminals, abol ished VIE inhibition but attenuated BVB inhibition only slightly. Thus nasa l stimulation inhibits BVB, and this inhibition is mediated exclusively by the trigeminal nerve and occurs principally at the pontomedullary level, al though the potential exists for contribution of the prejunctional mechanism . The inhibition of BVB might contribute to cardiovascular regulation assoc iated with protection from atmospheric hazards.