Korean J Otolaryngol-Head Neck Surg.
2003 Feb;46(2):115-119.
A Role of Nitric Oxide in the Enhancement of Neurogenic Inflammation with Capsaicin-Rechallenge in the Rat Nasal Mucosa
- Affiliations
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- 1Department of Otolaryngology, College of Medicine, Gyeongsang National University, Jinju, Korea. syjeon@nongae.gsnu.ac.kr
Abstract
- BACKGROUND AND OBJECTIVES
The role of neurogenic inflammation in the airways appears to protect the airways from various irritants in the inspired air. Enhanced NO production by inducible NO synthase (iNOS), which is expressed locally at the site of inflammation, has been implicated in the pathogenesis of inflammation. We studied to elucidate the role of NO in the pathogenesis of neurogenic inflammation in the nasal mucosa. MATERIAL AND METHOD: This study investigated the changes of microvascular leakage in the rat model of challenge/rechallenge with capsaicin, following the effects of a NOS inhibitor, NG-nitro-L-arginine methyl ester (L-NAME) and a substrate, L-arginine. And for more evident proofs, this study investigated the immunohistochemical localization of the expressed iNOS after capsaicin-challenge in the rat nasal mucosa. RESULTS: Capsaicin-rechallenge enhanced microvascular leakage in the nasal mucosa. Pretreatment with L-NAME inhibited the enhancement of neurogenic inflammation with capsaicin-rechallenge, and L-arginine reversed the inhibition of L-NAME. Strong immunohistochemical staining for iNOS was localized to inflammatory cells in the epithelial layer. CONCLUSION: Capsaicin or sensory neuropeptides released by capsaicin-challenge may induce the expression of iNOS in the nasal mucosa, and NO, produced by expressed iNOS, may mediate the enhancement of neurogenic inflammation with capsaicin-rechallenge.