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Intracisternal thyrotropin‐releasing hormone‐induced vagally mediated gastric protection against ethanol lesions: Central and peripheral mechanisms
Author(s) -
TACHÉ Y.,
YONEDA M.,
KATO K.,
KIRÁLY A.,
SÜTÖ G.,
KANEKO H.
Publication year - 1994
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 - 10.1111/j.1440-1746.1994.tb01298.x
Subject(s) - endocrinology , medicine , gastric acid , vagus nerve , thyrotropin releasing hormone , calcitonin gene related peptide , dorsal motor nucleus , nitric oxide , capsaicin , prostaglandin , stomach , neuropeptide , hormone , receptor , stimulation
Abstract The vagus is involved in mediating gastric cytoprotection and adaptive cytoprotection. However, the central and peripheral mechanisms through which the vagus expresses its action are still poorly known. Medullary thyrotropin‐releasing hormone (TRH) plays an important role in the vagal regulation of gastric function. The stable TRH analogue, RX 77368, micro‐injected into the cisterna magna or the dorsal motor nucleus (DMN) of the vagus at a dose that did not influence gastric acid secretion prevented gastric injury induced by intragastric administration of 60% ethanol in conscious or urethane‐anaesthetized rats. The cytoprotective action of TRH is mediated through vagal cholinergic release of prostaglandin E 2 (PGE 2 ). Prostaglandin E 2 action is unrelated to changes in gastric mucosal blood flow (GMBF). In addition, other peripheral mechanisms involve calcitonin gene‐related peptide (CGRP) contained in capsaicin sensitive afferent fibres and nitric oxide, both of which mediate the associated increase in GMBF induced by intracisternal injection of RX 77368. These data indicate that medullary TRH induces vagally mediated gastric protection against ethanol lesions. Its action is expressed through the muscarinic dependent release of PGE 2 and nitric oxide, and efferent function of capsaicin‐sensitive afferent fibres releasing CGRP.