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Central and peripheral vagal mechanisms involved in gastric protection against ethanol injury
Author(s) -
TACHÉ Y,
KANEKO H,
KAWAKUBO K,
KATO K,
KIRÁLY Á,
YANG H
Publication year - 1998
Publication title -
journal of gastroenterology and hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.214
H-Index - 130
eISSN - 1440-1746
pISSN - 0815-9319
DOI - 10.1046/j.1440-1746.1998.01736.x
Subject(s) - medicine , endocrinology , vasoactive intestinal peptide , peptide yy , calcitonin gene related peptide , gastric acid , cholinergic , regulation of gastric function , adrenomedullin , gastric mucosa , neuropeptide , stomach , receptor , neuropeptide y receptor
Activation of medullary thyrotropin‐releasing hormone (TRH), at a dose subthreshold to increase gastric acid secretion, protects the gastric mucosa against ethanol injury through vagal cholinergic pathways in urethane‐anaesthetized rats. Peripheral mediators involve the efferent function of capsaicin‐sensitive splanchnic afferents leading to calcitonin gene‐related peptide (CGRP)‐ and nitric oxide (NO)‐dependent gastric vasodilatory mechanisms. In addition, gastric prostaglandins participate in gastric protection through mechanisms independent of the stimulation of gastric mucosal blood flow and mucus secretion. Medullary TRH has physiological relevance in the vagal‐dependent adaptive gastric protection induced by mild (acid or ethanol), followed by strong, irritants. Additional neuropeptides, namely peptide YY (PYY), somatostatin analogues, CGRP and adrenomedullin, also act in the brainstem to induce a vagal‐dependent gastric protection against ethanol through interactions with their specific receptors in the medulla. Central PYY and adrenomedullin act through vagal cholinergic prostaglandins and NO pathways, while somatostatin analogue acts through vagal non‐adrenergic, non‐cholinergic vasoactive intestinal peptide and NO mechanisms. Although their biological relevance is still to be established, these peptides provide additional tools to investigate the multiple vagal‐dependent mechanisms which increase the resistance of the gastric mucosa to injury.