Nifedipine does not alter methacholine-induced bronchial reactivity.

Calcium ions have been shown to be involved in smooth muscle contraction and various secretory processes. Nifedipine, a calcium channel blocking drug, does not have any intrinsic bronchodilatory effect, but it has been suggested to possibly inhibit bronchial reactivity. Eight patients, with normal baseline pulmonary function studies and methacholine-induced bronchial reactivity, had a repeat metacholine challenge after nifedipine. Spirometry was obtained at baseline and three minutes after successive inhalations of normal saline and five, 15, 30, 50, 100 and 200 inhalation units of 0.5% methacholine. Plethysmographic lung volumes and airways resistance were measured at the start of the test and after the last inhalation of methacholine. The FEV1, FVC, MMEF and PEFR were reduced by an average of 35.6%, 20.6%, 54.4% and 30.6%, respectively, on the initial study, and by 35.4%, 20.5%, 54.8% and 34.5% after nifedipine. Airways resistance was increased by 249.3% in the initial study and by 265.7% after nifedipine. There was no statistical difference in baseline spirometry, spirometry obtained at any level of methacholine inhalation, or in airways resistance between the two studies. Despite comparable decreases in lung function, all patients were less symptomatic after receiving nifedipine. Nifedipine does not alter methacholine-induced bronchial reactivity. Until the role of nifedipine in asthma is better defined, caution should be used in prescribing nifedipine to asthmatic patients with heart disease, because their perception of airways resistance may be altered.