Nonopioid effects of beta-casomorphin-5 in guinea pig heart: alterations to the beta-adrenoceptor-G-protein complex and inhibition of myocardial responses to isoproterenol

Peptides. 1991 Mar-Apr;12(2):265-70. doi: 10.1016/0196-9781(91)90009-e.

Abstract

The influence of beta-casomorphin-5 on the beta-adrenoceptor complex in guinea pig heart membranes was studied by means of binding studies, G-protein investigations and isolated heart preparations. In nanomolar concentrations beta-CM-5 induced an increase in receptor affinity towards the agonist isoproterenol whereas the antagonist affinity was reduced. The isoproterenol-stimulated increase in cardiac contractility, moreover, is reduced by 10 nM beta-CM-5. Furthermore, beta-CM-5 was found to inhibit the isoproterenol-induced GDP/GTP exchange as well as the [35S]GTP[S] binding to guinea pig heart membranes, indicating an involvement of G-proteins. These findings suggest that low concentrations of beta-CM-5 modulate the functional properties of the myocardial beta-adrenoceptor-G-protein complex, presumably resulting in its desensitization. The observed effects of beta-CM-5 are not prevented by naloxone and, therefore, are nonopioid in nature.

MeSH terms

  • Amino Acid Sequence
  • Animals
  • Endorphins / chemistry
  • Endorphins / pharmacology*
  • GTP-Binding Proteins / metabolism
  • Guinea Pigs
  • Heart / drug effects*
  • In Vitro Techniques
  • Isoproterenol / pharmacology
  • Kinetics
  • Molecular Sequence Data
  • Myocardium / metabolism
  • Peptide Fragments / chemistry
  • Peptide Fragments / pharmacology*
  • Receptors, Adrenergic, beta / drug effects

Substances

  • Endorphins
  • Peptide Fragments
  • Receptors, Adrenergic, beta
  • beta-casomorphin 5
  • GTP-Binding Proteins
  • Isoproterenol