It has recently been shown that immunoglobulin (Ig)E facilitates the cholinergic bronchoconstrictor pathway in human tissue in vitro. However, whether this occurs in humans in vivo has not been clarified. In this study, the bronchodilator responses were examined to inhalation of a submaximal dose of the anticholinergic agent oxitropium bromide (600 microg) in normal and allergic subjects with various levels of total serum IgE. Values of the forced expiratory volume in one second (FEV1) for all subjects were greater than 80% of predicted, but were negatively correlated with serum IgE levels (p<0.01). Oxitropium bromide inhalation induced an increase in FEV1 that was significantly greater in allergic rhinitis patients with high serum IgE (155+/-20 mL (mean+/-SEM), p<0.05) than in healthy subjects (64+/-21 mL) or those with allergic rhinitis but low serum IgE (82+/-21 mL, p<0.05). In contrast, the effects of the inhaled beta2-adrenergic agent orciprenaline sulphate (2.25 mg) were not significantly different among the three groups. In conclusion, higher serum immunoglobulin E levels were correlated with lower values of the forced expiratory volume in one second, and anticholinergic agents, but not beta2-adrenergic agents, caused more pronounced bronchodilation in subjects with high than in those with low immunoglobulin E levels. These data suggest that serum immunoglobulin E may be one of the factors that determine the airway tone, possibly via cholinergic mechanisms.