Substance P and bradykinin stimulate plasma extravasation in the mouse gastrointestinal tract and pancreas

Michela Figini, Costanza Emanueli, Eileen F. Grady, Kimberly Kirkwood, Donald G. Payan, John Ansel, Craig Gerard, Pierangelo Geppetti, Nigel Bunnett

Research output: Contribution to journalArticlepeer-review

Abstract

Neurogenic inflammation is mediated by release of tachykinins from sensory nerves, which stimulate plasma extravasation from postcapillary venules. Because there are conflicting results regarding the importance of neurogenic inflammation in the gastrointestinal tract, we quantified plasma extravasation using Evans blue and identified sites of the leak using Monastral blue in the mouse. Substance P and bradykinin stimulated extravasation from postcapillary venules in the stomach, small and large intestine, pancreas, urinary bladder, trachea, and skin by two- to sevenfold by interacting with NK1 and B2 receptors, respectively. Stimulation of sensory nerves with capsaicin also induced extravasation. Capsaicin- and bradykinin-stimulated extravasation was attenuated by an NK1-receptor antagonist and is thus mediated by release of tachykinins and activation of the NK1 receptor. We conclude that 1) substance P stimulates extravasation in the gastrointestinal tract and pancreas of mice by interacting with the NK1 receptors, and 2) capsaicin and bradykinin induce plasma extravasation by stimulating tachykinin release from sensory nerves. Thus neurogenic mechanisms mediate inflammation in the gastrointestinal tract and pancreas of the mouse.

Original languageEnglish (US)
Pages (from-to)G785-G793
JournalAmerican Journal of Physiology - Gastrointestinal and Liver Physiology
Volume272
Issue number4 35-4
DOIs
StatePublished - Apr 1997

Keywords

  • kinins
  • neurogenic inflammation
  • sensory nerves
  • tachykinins

ASJC Scopus subject areas

  • Physiology
  • Hepatology
  • Gastroenterology
  • Physiology (medical)

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