Modulation of calcium homeostasis as a mechanism for altering smooth muscle responsiveness in asthma.

Airway hyperresponsiveness remains a defining characteristic of asthma. Traditional views assert that airway smooth muscle is an important structural effector cell in the bronchi that modulates bronchomotor tone induced by contractile agonists. New evidence, however, suggests that abnormalities in airway smooth muscle functions, induced by variety of extracellular stimuli, may play an important role in the development of airway hyperresponsiveness. Studies using isolated bronchial preparations or cultured cells show that inflammatory mediators and cytokines may alter calcium homeostasis in airway smooth muscle and render the cells nonspecifically hyperreactive to agonists.