Decreased mononuclear cell beta-adrenergic receptors in bronchial asthma: parallel studies of lymphocyte and granulocyte desensitization.

To assess the interaction of bronchial asthma and beta-agonist drugs, beta-adrenergic receptors were measured in human mixed leukocyte, mononuclear cell, and polymorphonuclear leukocyte cell membranes simultaneously. The densities and affinities of beta-adrenergic receptors were determined, by Scatchard analysis, with a potent beta-antagonist 125I-hydroxybenzylpindolol (125I-HYP) and compared among 12 nonatopic controls (group I), 13 mild asthmatics not taking drugs (group II), and eight asthmatics receiving long-term beta-agonist therapy (group III). Our findings were as follows. (1) Asthmatics not taking drugs (group II) have significantly lower mean mononuclear leukocyte beta-adrenergic receptor density (p less than 0.05) but no significant difference in mean polymorphonuclear leukocyte beta-adrenergic receptor density than the control group. (2) Asthmatics receiving long-term beta-agonist treatment (group III) had significantly lower mean beta-adrenergic receptor density in all three cell fractions (p less than 0.05). (3) Group I and II females had a higher mean beta-adrenergic receptor density in mixed leukocyte and polymorphonuclear cell fractions than males (p less than 0.05). (4) Terbutaline sulfate clearly caused desensitization of beta-adrenergic receptors in human leukocyte membranes in vivo. These results show that beta-adrenergic receptor density is influenced by cell type, beta-adrenergic agonist administration, and sex; they also show that bronchial asthma itself is associated with lower lymphocyte beta-receptor density.