Effect of hydrocortisone on beta-adrenergic receptors in lung membranes

Kenji Mano, Abdolah Akbarzadeh, Robert G. Townley

Research output: Contribution to journalArticle

104 Scopus citations

Abstract

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 [125]I-Iodohydroxybenzylpindolol ([125]I-HYP), a potent beta-adrenergic receptor antagonist. Specific binding of [125]I-HYP to rat lung membranes was saturable with 386 fmol of [125]I-HYP/mg protein at saturation. The apparent equilibrium dissociation constant of [125]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 [125]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 [125]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.

Original languageEnglish (US)
Pages (from-to)1925-1930
Number of pages6
JournalLife Sciences
Volume25
Issue number22
DOIs
StatePublished - Nov 26 1979

All Science Journal Classification (ASJC) codes

  • Biochemistry, Genetics and Molecular Biology(all)
  • Pharmacology, Toxicology and Pharmaceutics(all)

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