An increase in cytoplasmic Ca++ concentration can activate not only respiratory smooth muscles, but also mast cells, bronchial mucus glands, and the vagi. Altered control of cytoplasmic Ca++ may also be related to the development of bronchial hyperreactivity. Drugs that block Ca++ influx through specific Ca++ channels in plasma membranes are therefore expected to be effective in the treatment of asthma. Reports so far indicate that such drugs may enhance the action of bronchodilators and may offer partial protection against histamine- or methacholine-induced broncho-constriction; but they neither modify the basal bronchomotor tone of asthmatics nor reverse established bronchoconstriction. Calcium-channel blockers are also weak inhibitors of mediator release from mast cells except at high concentrations, which partly explains their inconsistent blocking activity in allergen-induced asthma. However, they are usually effective in preventing exercise-induced bronchoconstriction. They offer an alternative treatment for patients with chronic airflow obstruction who needβ-adrenergic blockade for coexisting cardiovascular problems. Limited data suggest that long-term use of calcium-channel blockers may benefit patients with chronic asthma. The therapeutic role of currently available Ca++-channel blockers is limited in asthma in view of their low potency; more specific airway Ca++ antagonists need to be developed.