The Ca2+requirements for excitation‐contraction coupling in smooth muscle may be satisfied from both intracellular and extracellular sources, the relative extent of use of which is both tissue‐ and stimulant‐dependent. Extracellular Ca2+is apparently mobilized through two separate pathways, receptor operated (ROC) and potential dependent (PDC) Ca2+channels. The latter process is sensitive to the Ca2+‐channel antagonists, a heterogeneous group of compounds including verapamil, nifedipine and diltiazem. Ca2+mobilization in respiratory smooth muscle is reviewed. The available evidence for this multiple stimulant‐sensitive system indicates that both intra‐ and extracellular sources of Ca2+are used. Data from bovine, canine and guinea pig tracheal muscle indicate, from studies of Ca2+‐dependence of response and Ca2+channel antagonist sensitivity, that the extent of use of extracellular Ca2+lies in the order K+histamine 5‐hydroxytryptamine>acetyl‐choline. The bronchodilator activity of the Ca2+channel antagonists is noted. Bronchial hyperreactivity is characterized by an increased sensitivity to a variety of stimulants including cold air, exercise, histamine and acetylcholine. The possible origins of this defect are noted. It is suggested that a defect in Ca2+mobilization or in the receptor ‐ Ca2+mobilization coupling process at the level of the smooth muscle may constitute an important underlying cause of bronchial hyperreactivity. Potential analogies to reactivity changes seen in hypertensive vascular smoo