Airway smooth muscle in asthma

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Abstract
One of the factors that may contribute to the exaggerated airway narrowing in asthma is an abnormality of the airway smooth muscle. This abnormality could take the form of an increase in the amount of muscle or an alteration in its pharmacological reactivity. The former could be due to either hypertrophy (an increase in individual muscle cell size) or hyperplasia (an increase in cell number). Changes in pharmacological reactivity that could be relevant to altered airway calibre could result from an increase in contraction or alternatively, a decrease in relaxation. Based on available evidence, the increase in smooth muscle bulk is probably the consequence of both hyperplasia and hypertrophy and several growth factors, inflammatory mediators and cytokines have been implicated. Asthmatic airway tissue is rarely available for in vitro pharmacological studies and evidence for enhanced contraction is limited. Recent evidence suggests that an abnormality in beta adrenoceptor function may contribute to impairment of relaxation, but further work needs to be done. Passive sensitization of non-asthmatic airways in vitro provides a good model for the study of the mechanisms underlying airway hyperresponsiveness, and will be the subject of more intensive study in the future.

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