Role of α2-adrenoceptors in the sympathetic inhibition of motility reflexes of guinea-pig ileum


  • Authors' current addresses P. J. Johnson: School of Chemical & Biomedical Sciences, Central Queensland University, Rockhampton, Queensland 4702, Australia.

    M. A. Vremec: Ludwig Research Institute, Parkville, Victoria 3052, Australia.

Corresponding author M. J. Stebbing: Department of Anatomy and Cell Biology, University of Melbourne, Parkville, Victoria 3010, Australia., Email:


  • 1Sympathetic regulation of the motility of guinea-pig ileum was investigated using mesenteric nerve (MN) stimulation to inhibit motility reflexes, in vitro.
  • 2Transmural electrical stimulation (5 Hz, 1 s) in intact intestinal segments, or inflation of a balloon against the mucosa in opened segments, evoked contractions of the circular and longitudinal muscles oral to the stimulus.
  • 3MN stimulation (10 Hz, 5 s) usually abolished contractions of the longitudinal and circular muscles evoked by either electrical or mechanical stimuli.
  • 4The inhibition was mimicked by UK14,304 (70-100 nm) and abolished by idazoxan (100 nm), revealing an enhancement of circular muscle contractions. There was no evidence for α2-receptors on the muscle, suggesting sympathetic inhibition was via the myenteric plexus.
  • 5Possible sites of action of noradrenaline released from sympathetic nerves were investigated using intracellular recordings from the circular muscle in a multichambered organ bath.
  • 6When in the stimulation chamber, UK14,304 depressed (by 50 %) excitatory junction potentials (EJPs) recorded oral to a distension stimulus, but did not affect inhibitory junction potentials (IJPs) recorded anal to the stimulus. When added to a chamber between the stimulus and recording chambers, UK14,304 depressed EJPs by 40 %, but did not alter IJPs. When in the recording chamber, UK14,304 depressed EJPs by 20 %, but had no effect on IJPs. IJPs were inhibited, however, when UK14,304 was applied to the whole bath.
  • 7It is concluded that sympathetic activity inhibits intestinal motility mainly via α2-adrenoceptors on ascending interneurons and intrinsic sensory neurons of the orally directed reflex pathway.