T he major resistance airways of human subjects are innervated by at least three different types of autonomic nerves. The specific physiologic “advantage” to this homeostatic system for regulation of bronchomotor tone is uncertain; however, some degree of bronchomotor tone results from parasympathetic innervation in all normal individuals. Asthma differs from the normal bronchoconstrictor response in both the severity of bronchoconstriction and by the apparent failure of normal homeostatic dilator systems to reverse the constrictor response. Through a variety of exogenous or endogenous stimuli, bronchoconstriction, which may be life-threatening, can occur in minutes to hours. Bronchospasm may ultimately remit spontaneously, and some “remissions” may last for many years between attacks. However, in all individuals with asthma, some degree of “occult” bronchoconstriction is usually apparent at all times. Asthma is a disease of diverse etiology. In this context, the disease is more correctly regarded as a syndrome, with many different stimuli promoting the final common event-bronchoconstriction accompanied by: 1) airway smooth muscle contraction, 2) mucous hypersecretion, and 3) regional inflammation of major resistance airways. Table 1 outlines some of the factors which may contribute to asthmatic bronchoconstriction. Most investigators agree that mediator release is often an important component in human bronchospasm. However, the precise method by which mediator release promotes airway smooth muscle contraction is a subject of considerable controversy (see below). Environmental stimuli contribute in a variety of ways to bronchospasm in susceptible individuals. Respiratory irritants (such as ozone or sulfur dioxide) may exacerbate asthmatic bronchoconstriction. Viral infection may have a similar effect. Some asthmatic events are iatrogenic, resulting from beta-adrenergic blockade or ingestion of prostaglandin synthetase inhibiting drugs. In contrast to