Nasal stimulation provokes hypertension and bradycardia. We report here that such stimulation inhibits baroreflex vagal bradycardia (BVB). In chloralose- and urethan-anesthetized, β-adrenergic receptor-blocked rats, the aortic depressor nerves were cut and electrically stimulated to induce BVB. Nasal application of smoke, warm distilled water, or cold or hot Ringer solution suppressed BVB, but application of warm Ringer solution did not. Smoke-induced inhibition was abolished by trigeminal but not olfactory denervation. Neither suprapontine decerebration nor C3 spinal cord transection affected the inhibition. Bradycardia induced by electrical stimulation of the peripheral cut end of the cervical vagus nerve (VIB) was suppressed by long-lasting smoke application. Intravenous prazosin, a proposed blocker of prejunctional inhibition of acetylcholine release from the vagus terminals, abolished VIB inhibition but attenuated BVB inhibition only slightly. Thus nasal stimulation inhibits BVB, and this inhibition is mediated exclusively by the trigeminal nerve and occurs principally at the pontomedullary level, although the potential exists for contribution of the prejunctional mechanism. The inhibition of BVB might contribute to cardiovascular regulation associated with protection from atmospheric hazards.
Acetylcholine release from rat atria can be regulated through an alpha 1-adrenergic receptor.