NITRIC-OXIDE IS A MEDIATOR OF NEUROGENIC VASCULAR EXUDATION IN THE NOSE

Rhinorrhea is a troublesome symptom of rhinitis seen commonly by otola ryngologists. The sources of nasal fluid production are glandular secr etions and exudation from submucosal blood vessels. This study was des igned to investigate the role of nitric oxide in neurogenically mediat ed vascular exudation in the nose. A rat model of the nasonasal reflex was developed in which one nasal cavity was challenged with histamine while albumin exudation was measured on the contralateral side. Hista mine challenge was associated with a significant rise in albumin leaka ge, indicating an increase in vascular permeability. Perfusion with a nitric oxide synthase inhibitor (N-nitro-L-arginine methyl ester (L-NA ME)) in the nasal cavity contralateral to nasal challenge was found to block albumin exudation on that side. This inhibition was overcome by the addition of L-arginine, the natural substrate of nitric oxide syn thase, to the perfusate. Treatment of the ipsilateral nasal cavity wit h L-NAME did not significantly decrease the contralateral response. Th ese findings indicate that NO is an important mediator of the effector arm of the nasonasal reflex that increases vascular permeability but is not involved in the sensory nerve afferent pathway Further elucidat ion of the role of NO in nasal physiology may lead to novel pharmacoth erapeutic approaches to the treatment of allergic and nonallergic rhin orrhea.