The production of nasal fluids serves an important role in the protect
ion of the upper respiratory system, but can also be a troublesome sym
ptom of rhinitis. The chief sources of nasal fluids are serous and muc
ous glandular secretion, epithelial goblet cell exocytosis, and exudat
ion from submucosal blood vessels. This study was designed to investig
ate the role of nitric oxide in neurogenically mediated nasal vascular
exudation and mucus secretion. A rat model of the naso-nasal reflex w
as developed in which one nasal cavity was challenged with histamine w
hile albumin and mucin production were measured in the continuously pe
rfused contralateral side. Histamine challenge was associated with a s
ignificant rise in contralateral albumin and mucin content. Perfusion
with a nitric oxide synthase inhibitor (L-NAME) in the nasal cavity co
ntralateral to nasal challenge was found to block albumin leakage, but
not mucin secretion, on that side. The inhibition of vascular exudati
on was overcome by the addition of L-arginine, the natural substrate o
f nitric oxide synthase, to the perfusate. Treatment of the ipsilatera
l nasal cavity with L-NAME did not significantly alter the contralater
al response. A high correlation was observed between albumin and mucin
concentration in the perfusate. These findings indicate that NO is a
mediator of the effector arm of the naso-nasal reflex that increases v
ascular permeability, but is not involved in the sensory nerve afferen
t pathway or in reflex mucin release. Further elucidation of the role
of NO in nasal physiology may lead to novel pharmacotherapeutic approa
ches to the treatment of allergic and nonallergic rhinitis.