Premium
The effect of platelet‐activating factor (PAF) on nasal airway resistance in healthy subjects is not mediated by nitric oxide
Author(s) -
Maniscalco M.,
Sofia M.,
Faraone S.,
Carratù L.
Publication year - 2000
Publication title -
allergy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.363
H-Index - 173
eISSN - 1398-9995
pISSN - 0105-4538
DOI - 10.1034/j.1398-9995.2000.00603.x
Subject(s) - nitric oxide , platelet activating factor , medicine , histamine , proinflammatory cytokine , bradykinin , basal (medicine) , nitric oxide synthase , rhinomanometry , placebo , mucous membrane of nose , endocrinology , platelet , allergy , methacholine , pharmacology , immunology , nose , inflammation , lung , surgery , respiratory disease , pathology , receptor , alternative medicine , insulin
Background : The nose is an important source of nitric oxide (NO) in man, but the relevance of NO production to the response to inflammatory mediators is not clear. Methods : In this study, we evaluated the effect of NO inhibition on nasal airway resistance (NAR) at baseline, after an acute challenge with platelet‐activating factor (PAF), a potent proinflammatory factor, and after an acute challenge with bradykinin (BK), both of which are mediators of allergic rhinitis in man. Eight healthy subjects were enrolled in the study. Nasal NO production was measured by the chemiluminescence method, and NAR was measured by active anterior rhinomanometry. Results : Basal nasal NO concentration was 500.6±115.6 ppb; it significantly decreased after topical administration of the NO‐synthase inhibitor L‐NAME, and the NO‐synthase substrate l ‐arginine caused a recovery in NO production. The administration of L‐NAME did not cause any change in basal NAR. In a double‐blind fashion, we performed nasal challenge with PAF and BK after topical pretreatment with either placebo or L‐NAME. After placebo pretreatment, both PAF and BK caused a significant increase in NAR (respectively, from 0.29±0.11 Pa s cm −3 to 0.75±0.21 Pa s cm −3 , and from 0.36±0.18 Pa s cm −3 to 0.71±0.25 Pa s cm −3 ; P <0.001, n =8). Pretreatment with L‐NAME did not prevent the PAF‐induced increase in NAR (from 0.31±0.10 Pa s cm −3 to 0.71±0.27 Pa s cm −3 ), whereas it prevented the BK‐induced increase in NAR (from 0.33±0.15 Pa s cm −3 to 0.43±0.16 Pa s cm −3 ). Conclusions : Topical administration of the NO‐synthase inhibitor L‐NAME at doses sufficient to decrease NO nasal production does not prevent the PAF‐induced increase in NAR, indicating that NO generation in vivo is not involved in the nasal response to PAF.