Decreased Beta-Adrenergic Receptors on Polymorphonuclear Leukocytes after Adrenergic Therapy

β-ADRENERGIC catecholamines, which modulate function of a variety of tissues, are assumed to act by initially binding to receptors on target-cell plasma membranes, thereby activating adenylate cyclase and stimulating generation of adenosine 3′:5′-monophosphate (cyclic AMP). In addition to activating adenylate cyclase, β-adrenergic agonists commonly have a second action — regulation of responsiveness of the target cells. Thus, continued treatment with such agonists often results in decreased cellular response. This self-regulation of target-cell responsiveness, variously termed refractoriness, desensitization and down-regulation, has been observed with catecholamines, as well as with a number of other hormonal agonists.1 2 3 For catecholamines, studies in several experimental . . .