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[Autonomic nerve receptors in the allergic nasal mucosa in human subjects and sensitized guinea pigs].

The purpose of this study is firstly to evaluate the abnormality of autonomic nerve receptors in human nasal mucosa in nasal allergy, and secondly to define whether this abnormality of these receptors are congenital or acquired. Autonomic nerve receptors in the nasal mucosa were measured using receptor binding assay in 14 subjects with perenial nasal allergy (ages 13-41, average age 35) and 13 subjects with chronic sinusitis (ages 15-44, average age 37).As radioligands we used [3H]-quinuclidinyl benzilate (QNB) for muscarinic cholinergic receptor, [3H]-prazosin for α1 adrenergic receptor and [3H]-dihydroalprenolol (DHA) for β adrenergic receptor. Compared with the nasal mucosa with chronic sinusitis an increased density (Bmax) of muscarinic cholinergic receptors (44% increased) and decreased densities of α1 adrenergic (37% decreased) and β adrenergic (41% decreased) receptors were observed in the nasal mucosa with nasal allergy. No differences were observed between both groupes in the dissociation constant (Kd) of each ligand to adrenergic and cholinergic receptors. The organ parasympathicotonia may explain the mucosal hyperreactivity to acetylcholine observed in subjects with nasal allergy. Decreased density of α1 adrenergic receptors will result in less constriction of the nasal vasculature in response to sympathetic stimulation. Decreased density of β adrenergic receptors may promote the release of chemical mediators from mast cells and basophils. We have already suggested that hypersensitivity of nasal mucosa observed in nasal allergy is nonspecific and that it is largely a result of antigen-antibody reaction. The organ parasympathicotonia in the nasal mucosa could be reproduced with TDI (toluene-2, 4-diisocyanate) sensitized guinea pigs which showed typical symptoms both of nasal allergy and bronchial asthma. But in the guinea pigs sensitized with bacterial crystalline α amylase, which appeared typical symptoms of bronchial asthma and no apparent symptoms of nasal allergy, the increased density of muscarinic cholinergic receptors could not be observed. These results suggest that the organ parasympathicotonia in the allergic nasal mucosa is not congenital, but is acquired secondarily to antigen-antibody reaction in the nasal mucosa.