Nasal nitric oxide inhibition prevents the bradykinin-induced increase in nasal airway resistance in normal humans

Background. Nose is an important source of nitric oxide (NO) in humans, but the importance of NO production in the regulation of nasal airway resistance (NAR) in basal conditions and in response to inflammatory mediators in not well known. In this study, the effect of NO inhibition on NAR at baseline and after an acute challenge with bradykinin (BK), a potent proinflammatory mediator that mimics many of the symptoms of rhinitis has been evaluated. Methods. Fifteen healthy subjects were enrolled in the study. Nasal NO production was measured by chemiluminescence method and NAR were measured by active anterior rhinomanometry. Results. Basal nasal NO concentration was 511.4 ± 112.6 ppb (n=9); it significantly decreased after L-NAME topically administrated (368.6 ± 80.6 ppb: n=9, p<0.001; L-arginine caused a recovery in NO production (498.2 ± 130.9 ppb). The administration of L-NAME did not cause any change in basal NAR (from 0.36 ± 0.18 Pa · sec · cm-3 to 0.38 ± 0.23 Pa · sec · cm-3; n=6). In a double blind fashion, nasal challenge with BK (1000 μg) was performed after topical pretreatment with either placebo or L-NAME. BK after placebo pretreatment caused a significant increase in NAR (from 0.38 ± 0.21 Pa · sec · cm-3 to 0.71 ± 0.30 Pa · sec · cm-3 p<0.05: n=6), whereas pretreatment with L-NAME significantly prevented the BK induced increase in NAR (from 0.36 ± 0.18 Pa · sec · cm-3 to 0.42 ± 19 Pa · sec. · cm-3). Conclusions. The conclusions is drawn that topical administration of the NO-synthase inhibitor L-NAME is able to decrease NO nasal production, but does not affect basal nasal airway resistance. NO inhibition by L-NAME prevents the BK- induced increase in NAR indicating NO release in vivo is involved in the nasal response to BK.