Airway caliber is primarily under the control of cholinergically innervated smooth muscle but it is also effected in pathological states by the tissue effects of chemical mediators released from mast cells, the hypersecretion of mucous glands, and the aggravation of airway narrowing by the vagus-mediated bronchoconstrictor reflex, and also by the ingress of inflammatory cells into the bronchial wall. The function of each of these cell types (smooth muscle, mast cells, mucous glands, vagus nerve, and inflammatory cells) is dependent upon Ca2+ ions. That is, agonist-induced smooth muscle contraction, antigen-induced mediator release from mast cells, mucous gland secretion, vagus nerve impulse initiation and conduction, and the movement of inflammatory cells are all Ca2+-dependent phenomena in which Ca2+ serves as the coupling agent between excitation and contraction and stimulus and secretion. Normally, all cells in the body maintain a very high inside-to-outside Ca2+ concentration gradient, the maintenance of which involves several mechanisms that pump calcium out of the cell. Calcium antagonists may inhibit the ingress of Ca2+ ions from the extracellular environment or may influence the availability of calcium ions from plasma membrane or subcellular organelles. Calcium antagonists have been shown to exert a beneficial effect in exercise-induced asthma and may possibly affect the release of chemical mediators from mast cells. The future of calcium antagonist therapy in the management of asthma remains to be determined.