Adrenergic Receptors in Pulmonary Medicine

All three subtypes of a1-adrenergic receptors (particularly the a1A-subtype) and all three subtypes of ^-adrenergic receptors are expressed in human lung at the mRNA level, but no major role in the regulation of human airway function has been described (49-53). Among the P-adrenergic receptors, P1- and P2-adrenergic receptors coexist in the human lung; the P3-subtype appears to be absent (53). P2-Adrenergic receptors are more abundant than P1-adrenergic receptors in all pulmonary cell types (except in pulmonary blood vessels) and are apparently the only subtype on airway smooth muscle cells (53). Accordingly, relaxation of airway smooth muscle is a prototypical function of P2-adrenergic receptors, and P2-selective agonists have been used for many years as bronchodilator drugs in asthma, chronic obstructive pulmonary disease, and other pulmonary conditions. Short-acting P-adrenergic agonists, such as salbutamol or terbutaline, are well established as acute bronchodilators, whereas long-acting P-adrenergic agonists, such as salmeterol or formoterol, are preferentially used alone or together with inhaled corticosteroids in prophylaxis and as suppressors of chronic bronchoconstriction (54,55). The expression and responsiveness of airway P2-adrenergic receptors can be regulated by a variety of factors that include genetics, age, disease states, and, possibly most important in therapeutics, drug treatment (43,56,57). The last includes desensitization on treatment with P-adrenergic agonists and sensitization (or prevention of desen-sitization) in patients treated with inhaled or systemically administered gluco-corticoids. P2-Adrenergic receptors on inflammatory cells, which have products that influence bronchial airway cell function and which are responsive to glu-cocorticoids, appear to show greater propensity for desensitization than do the receptors on airway smooth muscle (58,59).

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