Betamethasone increases the beta-adrenergic receptor density of human polymorphonuclear leukocytes.

Prolonged incubation (18h) of human polymorphonuclear leukocytes (PMNs) with betamethasone (BT) (10(-7) M) increased (3H)-DHA binding to human PMN membranes, apparently causing an increase in the number of beta-adrenergic receptors. Inhibition of this effect by cycloheximide (2 micrograms/ml) suggests that it is dependent on protein synthesis. BT had no effect on basal levels of cAMP in PMNs, but synergistically potentiated the increase in cyclic AMP (cAMP) induced by isoproterenol. Propranolol completely abolished the synergistic effect of BT plus isoproterenol, suggesting that the potentiating effect of BT on cAMP metabolism required the activation of beta-adrenergic receptors. Thus, BT increased the number of beta-adrenergic receptors in human PMN membranes and potentiated the cAMP changes induced by beta-agonists.