Inhibition of exercise-induced asthma by a calcium antagonist, nifedipine

Contraction of bronchial smooth muscle and release of mediators by mast cells are involved in asthmatic attacks and are calcium dependent. Therefore, we investigated the effects of a calcium antagonist, nifedipine, in asthma. Ten patients with asthma and documented exercise-induced bronchoconstriction exercised on 2 separate days after single-blind sublingual administration of 20 mg of placebo or nifedipine. The exercise-induced decreases in forced vital capacity, peak expiratory flow, and maximal expiratory flow after exhalation of 50 and 75% of the forced vital capacity were not modified on placebo but were prevented by nifedipine. Ten other asymptomatic patients with asthma and documented exercise-induced bronchoconstriction were studied at rest before and 45 min after nifedipine. The forced vital capacity, peak expiratory flow, and maximal expiratory flows were initially reduced and did not increase after nifedipine. Thus, nifedipine does not modify the basal bronchial tone of patients with asthma but does prevent exercise-induced asthma.