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.