Leukotriene antagonists (montelukast) are particularly effective as controllers before exposure to an allergen (Leff 1998). The same applies to the treatment of bronchoconstriction induced by physical exertion or cold air (Richter 2000). Montelukast binds to the cysteinyl leuko¬triene-1 receptor, where it prevents leukotriene from binding. Leukotrienes play a key role as mediators in inflammatory processes. By binding to the receptor they cause, among other things, edema, damage to the bronchial epithelium and bronchoconstriction. Accordingly, in addition to its anti-inflammatory activity montelukast brings about bronchial dilation. The safety and efficacy of the drug in children have been well documented (Knorr 1998). Hence montelukast is approved for the treatment of bronchial asthma in children (over six months of age). As with other antiasthmatic drugs, there are responders and nonresponders to leukotriene receptor antagonists. The proportion of nonresponders to montelukast among children is esti¬mated to be 30% to 40%. At present the only way to distinguish non-responders from responders is to run a treatment trial for several weeks. If the symptom score falls, if the use of beta2 sympathomimetics is reduced, if pulmonary function and/or the quality of life improves, it is assumed that the patient is a responder. This method is not only tedious but also unsafe, since a change is the aforementioned parameters could occur spontaneously, without this being reliably attributable to the influence of the drug. In the planned study approximately 30 children with asthma of GINA classes 2 and 3 will be regularly examined for pulmonary function, symptom score and nitrogen monoxide (NO). First, however, the acute pharmacologic effect of a single dose of montelukast will be deter¬mined over a period of four hours by measuring pulmonary function and levels of exhaled nitrogen monoxide (NO).