EVIDENCE THAT ENHANCED NASAL REACTIVITY TO BRADYKININ IN PATIENTS WITH SYMPTOMATIC ALLERGY IS MEDIATED BY NEURAL REFLEXES

Objective: The aim of this study was to determine whether allergic inf lammation induces nasal hyperreactivity to bradykinin by enhancing neu ronal responsiveness. Methods: We compared the response to localized, unilateral nasal challenge with bradykinin in patients with perennial allergic rhinitis and nonallergic subjects, and in patients with seaso nal allergic rhinitis challenged in and out of season. Weights of secr etions from each nostril were recorded, and levels of albumin and lact oferrin in secretions recovered from each nostril were assayed. Contra lateral administration of atropine (0.32 mg) was used to evaluated the role of cholinergic reflexes in nasal hyperresponsiveness to bradykin in. Results: In patients with symptomatic allergy, bradykinin induced greater symptoms scores than in asymptomatic atopic or nonallergic con trol subjects. Moreover, bradykinin caused sneezing in a majority of p atients with symptomatic allergy but in none of the asymptomatic atopi c or nonallergic control subjects. Only patients with symptomatic alle rgy showed dose-dependent bilateral increases in secretion weights and levels of the serous glandular maker, lactoferrin. In contrast, brady kinin induced similar increases in ipsilateral, but not contralateral, levels of albumin in all patient populations. Atropine inhibited cont ralateral secretion and lactoferrin production (p < 0.05) in patients with symptomatic allergy. Conclusion: The induction of sneezing and of atropine-inhibitable contralateral glandular secretion demonstrates t hat allergic inflammation causes nasal hyperreactivity to bradykinin, at least in part, by enhancing neuronal responsiveness.