Background: Atopic individuals have previously been shown to have an autonomic imbalance consisting of heightened cholinergic responsiveness in the lung, skin, and eyes, and beta-adrenergic hyporesponsiveness in the lungs, eyes, and vasculature. This array of abnormalities is often accompanied by nonspecific bronchial hyperresponsiveness, as well as alpha-adrenergic hyperresponsiveness in individuals with asthma.
Methods: To determine whether atopic individuals have intrinsic nasal airway hyperresponsiveness to methacholine, 21 nonatopic subjects and 37 subjects with allergic rhinitis were studied. All subjects were studied out of their allergy seasons, and all allergy-related medications were discontinued before the study began. Subjects underwent nasal challenge with methacholine (1 to 25 mg), and lavaged nasal secretions were analyzed for total protein, the plasma marker albumin, and the glandular marker lactoferrin.
Results: Atopic subjects demonstrated increased glandular responsiveness to methacholine as evidenced by an increase in the secretion of lactoferrin in response to individual doses of methacholine. Although the maximal lactoferrin secretion did not increase, glandular sensitivity to methacholine was heightened because the dose of methacholine required to induce lactoferrin secretion achievable by 60% of the study population was significantly lower in the atopic group. The volume of lavaged secretions recovered and congestion scores were also higher in the atopic group as compared with the normal control group.
Conclusions: These data strongly suggest that atopic individuals have intrinsic nasal glandular hyperresponsiveness to cholinergic stimulation.