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Corticosteroids

Potential ß₂-Agonist and Anticholinergic Interactions in Chronic Obstructive Pulmonary Disease

Respiratory Science, GlaxoSmithKline, Greenford, Middlesex, United Kingdom

Correspondence and requests for reprints should be addressed to Malcolm Johnson, Ph.D., Global Director, Respiratory Science, GlaxoSmithKline, Greenford Road, Greenford, Middlesex UB6 0HE, UK. E-mail: malcolm.w.johnson{at}gsk.com

Corticosteroids are often used in combination with ß₂-agonist and anticholinergic bronchodilators in the treatment of chronic obstructive pulmonary disease (COPD). Corticosteroids activate the ß₂-receptor gene, increasing receptor number and decreasing desensitization. Long-acting ß₂-agonists prime the glucocorticoid receptor and enhance nuclear translocation via activation of CCAAT enhancer binding protein-. Corticosteroids can also increase prejunctional auto-inhibitory M₂-receptor gene expression in airway smooth muscle. There is evidence of a synergistic inhibition of cytokine and chemokine release from alveolar macrophages, epithelial cells, and mucosal glands and enhanced respiratory cytoprotection against viral and bacterial infection when a corticosteroid is combined with salmeterol. In airway smooth muscle, corticosteroids inhibit the contractile effects of acetylcholine, whereas M₂-receptor antagonism increases the relaxant activity of isoproterenol. Complementary interactions between corticosteroids and long-acting ß₂-agonists and between corticosteroids and anticholinergic bronchodilators may be important if these drugs are combined in the treatment of COPD.

Key Words: ß₂-receptors • combination therapy • muscarinic receptors

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