Age-dependency of alpha- and beta-adrenoceptors on thrombocytes and lymphocytes of asthmatic and nonasthmatic children.

Among the possible mechanisms which may cause wheezing or asthmatic episodes a genetically determined beta-adrenoceptor blockade and a hyperresponsiveness of alpha-adrenoceptors has been postulated. Evidence to support this hypothesis stems from an increased bronchial sensitivity to beta-blockers, a reduced formation of cyclic AMP in response to beta-adrenergic stimulation and enhanced alpha-adrenergic responses in asthmatic subjects. The recent development of techniques for measuring the specific, high-affinity binding of radiolabeled alpha- and beta-adrenergic antagonists made it possible to study alpha- and beta-adrenoceptors in vitro. Based upon the assumption that a change in the number and/or affinity of adrenergic receptors might be a general phenomenon, we have performed alpha- and beta-receptor binding studies on lymphocytes and platelets from wheezing infants and asthmatic children as well as of infants, children, and adults not suffering from these diseases. Using 125[I]-cyanopindolol (ICYP) and 3[H]-yohimbine (HYOH) as highly specific ligands for alpha- and beta-adrenoceptors, the following results were obtained: Lymphocytes and platelets from control subjects and asthmatics bound similar amounts of ICYP and HYOH and thus showed no differences either in the number or the affinity of alpha- and beta-adrenoceptors. Lymphocytes and platelets of wheezing and nonwheezing infants also bound the same amounts of the radioligands. In asthmatic children receiving 4 X 2 puffs salbutamol beta-adrenoceptors were down-regulated and this may mimic beta-adrenoceptor blockade. When subjects were divided into four categories according to age (0-5, 5-10, 10-20 years, adults) the number of beta-adrenoceptor binding sites showed an age-dependent increase.(ABSTRACT TRUNCATED AT 250 WORDS)