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Corticosteroid-Induced Differential Regulation of β-Adrenergic Receptors in Circulating Human Polymorphonuclear Leukocytes and Mononuclear Leukocytes^*

ALBERT O. DAVIES and ROBERT J. LEFKOWITZ

Howard Hughes Medical Institute Laboratory, Departments of Medicine and Biochemistry, Duke University Medical Center Durham, North Carolina 27710

Address requests for reprints to: Dr. Albert O. Davies, Department of Medicine, Division of Pulmonary Disease, Duke University Medical Center, Durham, North Carolina 27710.

A method of reproducibly measuring human leukocyte β-adrenergic receptor density and affinity has been developed and applied to the study of receptor regulation in man. The method has the advantages of using a membrane preparation which binds highly specifically and employing techniques such as using low concentrations of [³H] dihydroalprenolol, analyzing the data by computer modelling techniques, and providing data from both granulocytes and lymphocytes in the same individual to minimize measurement errors. Using this methodology,human β-adrenergic receptor regulation is examined. Cortisone acetate was found to induce an acute rise in granulocyte βadrenergic receptor density and adenylate cyclase activity and an acute fall in lymphocyte βadrenergic receptor density. This potentially differential regulation of a single receptor subtype in two lines of leukocytes has important implications for the study of receptor regulation in man using leukocyte models.

^* This work was supported in part by a NIH National Research Service Award (1-F32-HL-05805-1) from the Heart and Lung Institute and HEW Grants HL-16037 and HL-20339.

Investigator, Howard Hughes Medical Institute.

Received February 25, 1980.

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