Associated with airways extending from the trachea to the terminal bronchioles is a layer of smooth muscle. In the trachea, smooth muscle constitutes a fraction of the circumference and connects the ends of incomplete cartilage rings. The fractional contribution of smooth muscle increases in lower airway segments such that the bronchi and bronchioles are encircled by a layer of smooth muscle. The length of the smooth muscle cells at any particular time determines the circumferential length of the airway and thereby influences airway caliber. Smooth muscle contraction (shortening) reduces airway caliber (causes bronchoconstriction) which increases resistance to airflow and makes breathing or ventilation more difficult. Smooth muscle relaxation (lengthening), on the other hand, decreases the work associated with ventilation by increasing airway caliber (causing bronchodilation) and reducing resistance to airflow.

A variety of agents act on airway smooth muscle to affect its state of contraction (tone), the majority of which act by specific receptors on the smooth muscle cell (Table 2). Bronchodilator drugs may be agonists of receptors subserving airway smooth muscle relaxation (e.g., b2-adrenoceptor agonists) or antagonists of receptors mediating airway smooth muscle concentration (e.g., muscarinic cholinoceptor antagonists). Other drugs may exert actions on cellular mechanisms that influence the intracellular processes of airway smooth muscle contraction or relaxation (e.g., xanthine derivatives). The sites of action of these drugs are shown in Fig. 2.

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