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A calcium antagonist, nifedipine, modifies exercise-induced asthma
Thorax
|October 1, 1981
Summary
Nifedipine significantly reduced exercise-induced bronchoconstriction in asthma patients by inhibiting mast cell mediator release and slightly reducing bronchial smooth muscle contractility. This suggests a potential therapeutic role for nifedipine in managing asthma symptoms.
Area of Science:
- Pharmacology
- Respiratory Medicine
- Immunology
Background:
- Exercise-induced bronchoconstriction (EIB) is a common asthma symptom.
- Nifedipine, a calcium channel blocker, is known to affect smooth muscle and secretory cells.
Purpose of the Study:
- To investigate the effect of sublingual nifedipine on exercise-induced bronchoconstriction in extrinsic asthmatic subjects.
- To explore nifedipine's impact on mast cell mediator release and bronchial smooth muscle contractility.
Main Methods:
- Double-blind, randomized, placebo-controlled study in eight extrinsic asthmatic subjects.
- Treadmill exercise tests performed 30 minutes after 20 mg sublingual nifedipine or placebo.
- Measurements included peak expiratory flow, plasma histamine levels, and histamine challenge dose.
Main Results:
- Nifedipine significantly reduced the maximum fall in peak expiratory flow post-exercise compared to placebo (36.0% vs 56.5%).
- Nifedipine prevented the exercise-induced rise in plasma histamine, suggesting inhibition of mast cell mediator release.
- Nifedipine increased the dose of inhaled histamine required to cause bronchoconstriction, indicating a mild inhibitory effect on bronchial smooth muscle.
Conclusions:
- Sublingual nifedipine effectively attenuates exercise-induced bronchoconstriction in extrinsic asthmatics.
- Nifedipine appears to work by inhibiting mast cell mediator release and, to a lesser extent, reducing bronchial smooth muscle responsiveness.
- These findings suggest nifedipine may be a viable option for managing asthma symptoms related to exercise.