Action of corticosteroids on beta-adrenergic receptors. Clinical aspects.
Inhaled beta 2-stimulants are the most effective drugs for acute asthma attacks. This is probably due to functional antagonism against a large variety of possible asthma mediators. A defect in beta-receptor function is not the cause of asthma but treatment with beta 2-stimulants induces a down-regulation of beta-receptors and beta-receptor function outside the lung. There is, however, no convincing evidence that tachyphylaxis of clinical importance to the bronchodilating effect occurs in asthmatics receiving normal doses of beta 2-receptor stimulants. A slight rebound increase of bronchial hyperreactivity has, however, been demonstrated 12 to 23 h after stopping regular treatment. This may be due to slight tachyphylaxis not visible in normal lung function tests. Inhaled steroids should be given to all asthmatics needing regular inhaled beta 2-agonist treatment, at least to adults. Steroids not only seem to reduce bronchial inflammation and hyperreactivity, and thereby the distribution of inhaled drugs, but also attend to reverse beta 2-receptor subsensitivity.
Svedmyr
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Department of Clinical Pharmacology, Sahlgren's University Hospital, Gothenburg, Sweden.
D000318:Adrenergic beta-Agonists / Q000627:therapeutic use; D000818:Animals; D001249:Asthma / Q000188:drug therapy* / Q000503:physiopathology; D004359:Drug Therapy, Combination; D005938:Glucocorticoids / Q000494:pharmacology* / Q000627:therapeutic use; D006801:Humans; D011943:Receptors, Adrenergic, beta / Q000187:drug effects* / Q000502:physiology; D013618:Tachyphylaxis / Q000502:physiology
D000318:Adrenergic beta-Agonists; D005938:Glucocorticoids; D011943:Receptors, Adrenergic, beta