EFFECT OF HYDROCORTISONE ON BETA-ADRENERGIC RECEPTORS IN LUNG MEMBRANES

Glucocorticoids potentiate .beta.-adrenergic stimulation of cardiovascular and airway tissues. The effect of glucocorticoids on the number and affinity of .beta.-adrenergic receptors in animal lung tissues was studied by a direct binding technique using 125I-iodohydroxybenzylpindolol (125I-HYP), a potent .beta.-adrenergic receptor antagonist. Specific binding of 125I-HYP to rat lung membranes was saturable with 386 f[femto]mol of 125I-HYP/mg protein at saturation. The apparent equilibrium Kd of 125I-HYP for .beta.-receptors was 221 nM. Chronic administration of hydrocortisone increased the density of .beta.-adrenergic receptors by 70% from 386-657 fmol/mg with some decrease in the affinity of 125I-HYP for .beta.-adrenergic receptors. Adrenalectomy produced a 29% fall in the number of .beta.-adrenergic receptors without altering the affinity of 125I-HYP for .beta.-receptors, and this change was reversed by exogenous administration of hydrocortisone. Apparently, glucocorticoids may participate in regulating the density of .beta.-adrenergic receptors and may potentiate .beta.-adrenergic receptor stimulation, by increasing .beta.-receptor density in tissue membranes.