Reduction by N^G‐nitro‐L‐arginine methyl ester (L‐NAME) of antigen‐induced nasal airway plasma extravasation in human subjects in vivo

Abstract

In non-allergic subjects, histamine induced a reduction of minimal nasal cross-sectional area (Amin) and an increase in albumin release into nasal lavage. The effect of histamine on albumin release was inhibited by pretreatment with NG-nitro-L-arginine methyl ester (L-NAME), 1 jmol but not by D-NAME, 1 jpmol.L-NAME, 1 and 10 pmol, did not inhibit the histamine-induced reduction of Amin. In subjects allergic to grass pollen, antigen challenge induced a reduction in Amin that was not changed by pretreatment with L-NAME, and an increase in albumin release that was inhibited by L-NAME, 1 jimol. The data support a role for nitric oxide in mediating plasma extravasation in the nose induced by antigen challenge or histamine.

Localization of Nitric Oxide Synthase in Human Nasal Mucosa with Nasal Allergy

“…NO plays an important role in the regulation of a wide variety of upper respiratory functions, including vascular dilatation (23) and plasma extravasation (24). We suggest that large amounts of NO induced by iNOS could be responsible for certain symptoms of nasal allergy.…”

Effect of nitric oxide inhibition on nasal airway resistance after nasal allergen challenge in allergic rhinitis

“…Indeed, we did not find any effect of L-NAME pretreatment on early NAR increase induced by the allergen challenge. However, in subjects allergic to grass pollen, Dear et al [19] have demonstrated that topical administration of L-NAME was able to partially inhibit plasma extravasion by antigen challenge or histamine, while not preventing minimal cross section area decrease induced by nasal allergen challenge. Accordingly our data support their concept that nasal blockage following the allergen could occur by a mechanism independent of NO generation.…”

Regulation of Cys-Based Protein Tyrosine Phosphatases Via Reactive Oxygen and Nitrogen Species in Mast Cells and Basophils

“…physiological and pathological responses, including immune [57] and nasal airway response [58]. Important molecular targets of NO are various kinases, including p21ras, PKB, SEK1, JNK1, JNK2, SAPK, Erk1, Erk2, PI3K, Jak3, Tyk2, STAT5, Src, Raf-1 kinase, FAK and creatine kinase (reviewed in [49]), and PTPs (this review).…”