The pathophysiologic processes that contribute to airway obstruction in asthma involve Ca2+-dependent excitation-contraction and stimulus-secretion coupling mechanisms. The emergence of new compounds that specifically inhibit Ca2+ flux across membrane ionic channels has stimulated widespread interest in the therapeutic potential of these agents in asthma. Studies with these agents in relevant in vitro test systems and animal models, however, have yielded conflicting results and have thus far failed to furnish strong support for a therapeutic role. In human studies, these agents have been found to inhibit exercise-induced bronchospasm, but their ability to inhibit the effects of other stimuli and to dilate airways is equivocal. In general, clinical trials with currently approved drugs--diltiazem, nifedipine, and verapamil--are limited by potency, formulation, and side effects of these agents. What future role, if any, Ca2+ channel antagonists will have in the treatment of asthma is likely to depend on the development of newer agents with greater tissue selectivity at the level of airway smooth muscle and mast cells.