Glucagon-like peptide-1 receptor stimulation increases blood pressure and heart rate and activates autonomic regulatory neurons. Academic Article uri icon

Overview

abstract

  • Glucagon-like peptide-1 (GLP-1) released from the gut functions as an incretin that stimulates insulin secretion. GLP-1 is also a brain neuropeptide that controls feeding and drinking behavior and gastric emptying and elicits neuroendocrine responses including development of conditioned taste aversion. Although GLP-1 receptor (GLP-1R) agonists are under development for the treatment of diabetes, GLP-1 administration may increase blood pressure and heart rate in vivo. We report here that centrally and peripherally administered GLP-1R agonists dose-dependently increased blood pressure and heart rate. GLP-1R activation induced c-fos expression in the adrenal medulla and neurons in autonomic control sites in the rat brain, including medullary catecholamine neurons providing input to sympathetic preganglionic neurons. Furthermore, GLP-1R agonists rapidly activated tyrosine hydroxylase transcription in brainstem catecholamine neurons. These findings suggest that the central GLP-1 system represents a regulator of sympathetic outflow leading to downstream activation of cardiovascular responses in vivo.

publication date

  • July 1, 2002

Research

keywords

  • Autonomic Nervous System
  • Blood Pressure
  • Heart Rate
  • Receptors, Glucagon
  • Venoms

Identity

PubMed Central ID

  • PMC151031

Scopus Document Identifier

  • 0036307872

Digital Object Identifier (DOI)

  • 10.1172/JCI15595

PubMed ID

  • 12093887

Additional Document Info

volume

  • 110

issue

  • 1