It has been observed that glucocorticoids potentiate beta-adrenergic stimulation of cardiovascular and airway tissues. In order to investigate the mechanism of this potentiating action, we examined the effect of glucocorticoids on the number and affinity of beta-adrenergic receptors in animal lung tissues, by a direct binding technique using I-Iodohydroxybenzylpindolol (I-HYP), a potent beta-adrenergic receptor antagonist. Specific binding of I-HYP to rat lung membranes was saturable with 386 fmol of I-HYP/mg protein at saturation. The apparent equilibrium dissociation constant of I-HYP for beta-receptors was 221 nM. Chronic administration of hydrocortisone increased the density of beta-adrenergic receptors by 70% from 386 fmol to 657 fmol/mg with some decrease in the affinity of I-HYP for beta-adrenergic receptors. By contrast, adrenalectomy produced a 29% fall in the number of beta-adrenergic receptors without altering the affinity of I-HYP for beta-receptors, and this change was reversed by exogenous adminstration of hydrocortisone. The present study suggests that glucocorticoids may participate in regulating the density of beta-adrenergic receptors, and may potentiate beta-adrenergic receptors stimulation, at least in part by increasing beta-receptor density in tissue membranes.
All Science Journal Classification (ASJC) codes
- Biochemistry, Genetics and Molecular Biology(all)
- Pharmacology, Toxicology and Pharmaceutics(all)