5 Airway Smooth Muscle Cells Structure and Function
Abstract
The responsiveness in airway smooth muscle (ASM) is determined by the interplay of myogenic and neural controls, modulated by inflammatory and other stimuli. However, the functional range and extent of the modulation of myogenic and neural control systems have not been clarified yet. The structures controlling airway muscle at a cellular level are gap junctions, other cell–cell junctions, nerve endings in muscle, and sometimes nearby immune cells. There is a wide variation among species in nerve density in the trachea, with small animals having a notably higher density than humans. There is also considerable variation in the nerve density among different components of the airway musculature; in humans and dogs, the bronchi are much more densely innervated and the bronchi contain a significant component of their innervation from nerves that appear to be adrenergic. The canine ASM also exhibits some structural features that suggest the importance of internal Ca2+ stores. Mechanical stress is not transmitted among bronchial cells by the way of intermediate contacts, which are sparse, especially in bronchi. This may allow more movement of cells relative to one another and may also account for the highly irregular muscle-cell profiles. As a result, mechanical stress during breathing and with bronchoconstriction/bronchodilation may be transmitted mainly by gap junctions, explaining their rapid turnover.