GLP-1 stimulates secretion of macromolecules from airways and relaxes pulmonary artery

Am J Physiol. 1993 Oct;265(4 Pt 1):L374-81. doi: 10.1152/ajplung.1993.265.4.L374.

Abstract

Recent data revealed the existence of specific receptors for glucagon-like peptide-1(7-36)amide (GLP-1) on rat lung membranes. Utilizing slide-mount autoradiography of fresh frozen lung tissue sections, we have localized binding sites for GLP-1 on mucous glands in the trachea and on vascular smooth muscle of the pulmonary artery. When tracheas were incubated in a modified Ussing chamber, the addition of GLP-1 to the submucosal side increased 35S-sulfate-labeled macromolecule secretion (191 +/- 12% above basal, P < 0.005). The optimal secretory response elicited by GLP-1 was approximately 23% of the maximal secretory response after a maximal acetylcholine stimulation. Other proglucagon-derived peptides such as glucagon, oxyntomodulin, and GLP-2 had no effect. In isolated rings of arteries, GLP-1 (10(-8) to 10(-5) M) induced a dose-dependent and time-reversible relaxation of preconstricted arteries. In a preparation with denuded epithelium, GLP-1 lost its effect. In conclusion, GLP-1 might represent another neuropeptide that acts as neurotransmitter of the peptidergic, nonadrenergic-noncholinergic nervous system that innervates the airways.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Autoradiography
  • Glucagon / metabolism
  • Glucagon / pharmacology*
  • Glucagon-Like Peptide 1
  • In Vitro Techniques
  • Macromolecular Substances
  • Male
  • Mucus / metabolism
  • Peptide Fragments / metabolism
  • Peptide Fragments / pharmacology*
  • Protein Precursors / metabolism
  • Protein Precursors / pharmacology*
  • Pulmonary Artery / drug effects*
  • Pulmonary Artery / metabolism
  • Rats
  • Rats, Sprague-Dawley
  • Trachea / metabolism*
  • Vasodilation*

Substances

  • Macromolecular Substances
  • Peptide Fragments
  • Protein Precursors
  • Glucagon-Like Peptide 1
  • Glucagon