Beta2-adrenergic agonists ( β2-agonists) play a pivotal role in the acute and chronic management of asthma. Their major action on the airways is the relaxation of smooth muscle cells. In addition to their bronchodilator properties, β2-agonists may have other effects through their activation of β2-receptors expressed on resident airway cells such as epithelial cells and mast cells and circulating inflammatory cells such as eosinophils and neutrophils. These non-bronchodilator activities of β2-agonists may enhance their efficacy in the management of asthma. In pre-clinical studies, the anti-inflammatory effects of β2-agonists are demonstrated through their stabilizing effect on mast cells and their inhibition of mediator release from eosinophils, macrophages T-lymphocytes, and neutrophils. In addition, β2-agonists may inhibit plasma exudation in the airway, the release of neuropeptides from sensory nerves, and mediator release from epithelial cells. These in vitro observations are not as clearly demonstrated in clinical trials, which may be explained by the rapid desensitization of β2-adrenergic receptors on airway inflammatory cells. The regular use of short-acting β2-agonists alone has been shown to have deleterious effects on asthma control. Therefore, short-acting agents should only be used when needed for rescue of acute symptoms. Monotherapy with long-acting β2-agonists has also been associated with poor asthma control. However, when given concomitantly with inhaled corticosteroids, β2-agonists may potentiate the antiinflammatory effect of corticosteroids, improve asthma control and prevent exacerbations.
Keywords: asthma, adrenergic receptors, inflammatory cells, agonists, asthma therapy, airway inflammation
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