The most attractive "adrenergic theory" has proposed that in asthmatic patients the bronchial hyperreactivity might be caused by a decreased beta-receptor and an increased alpha-receptor responsiveness. Based upon the assumption that an abnormality of adrenergic receptors might be a general phenomenon, we have performed receptor-binding studies on lymphocytes and thrombocytes from asthmatic children who had and had not undergone treatment with beta-receptor agonists and/or glucocorticoids. Iodo-cyano-pindolol and tritium-labeled yohimbine were used as beta- and alpha-receptor ligands. The following results have been obtained: 1) The number and affinity of alpha- and beta-adrenoceptors on thrombocytes and lymphocytes showed no significant differences in asthmatic children and their age-matched controls. 2) In vivo treatment of asthmatic children with beta-receptor agonists immediately reduced the number of beta-receptors ("down regulation"). A reversal of the number of beta-receptors occurred within 1 day after cessation of the therapy. Although it appeared that some asthmatics with severe asthma have a reduced number of beta-receptors, in vivo treatment with beta-receptor agonists thus might mimic a beta-receptor blockade. 3) High-dose treatment with glucocorticoids increased the number of beta-receptors but left the alpha-receptors unaffected.