Exposure to antigen by inhalation challenge may produce airway constriction in patients with allergic asthma. To examine the role of reflex bronchoconstriction mediated by the vagus nerve in the antigen-induced airway response, we compared the responses of 6 asthmatic volunteers to inhaled ragweed antigen alone and to antigen given after pretreatment with atropine sulfate, a parasympathetic blocking agent. We found significant increases in airway resistance, limitation of parasympathetic blocking agent. We found significant increases in airway resistance, limitation of forced expiratory flow, increases in lung volumes, and alterations in the distribution of inspired gas after antigen was given. When subjects were pretreated with atropine, we found a mean increase in the 1-sec forced expired volume of 0.380 liter (P less than 0.025) and a mean increase in specific airway conductance of 0.067 sec-1-cm H2O-1 (P less than 0.005). Atropine pretreatment did not prevent the responses to antigen in our subjects. After atropine pretreatment subjects began the antigen challenge with better pulmonary function and at a given antigen dose maintained a better level of function compared to when antigen was given alone. Differences in the absolute level of pulmonary function between the two challenges became smaller with the administration of larger antigen doses. We conclude that reflex bronchospasm involving postganglionic efferent parasympathetic nerve pathways is not a major component of the response to inhaled antigen in human allergic asthma.