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Enhancement by intracerebroventricular thyrotropin‐releasing hormone of indomethacin‐induced gastric lesions in the rat
Author(s) -
MaedaHagiwara Masaki,
Watanabe Hiroshi,
Watanabe Kazuo
Publication year - 1983
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1983.tb10065.x
Subject(s) - bethanechol , thyrotropin releasing hormone , endocrinology , medicine , phentolamine , gastric mucosa , gastric acid , atropine , aspirin , hormone , secretion , chemistry , stomach , stimulation , receptor , muscarinic acetylcholine receptor
1 Effects of the intracerebroventricular thyrotropin‐releasing hormone (TRH) on gastric mucosa were studied in rats. 2 TRH (3 and 10 μg rat −1 i.c.v.) produced slight gastric lesions and also aggravated indomethacin‐, aspirin‐ or 5‐hydroxytryptamine (5‐HT)‐induced gastric lesions, while restraint and cold stress‐induced lesions were not influenced by TRH. 3 Bethanechol used at a dose sufficient to produce acid secretion did not influence the gastric mucosa in intact or indomethacin‐treated rats. 4 Enhancement of indomethacin‐induced gastric lesions by TRH was not inhibited to any significant degree by atropine 0.1 mg kg −1 s.c., which prevented TRH‐induced gastric acid secretion, but tended to be inhibited by phentolamine, 2.5 mg kg −1 i.p. 5 It is concluded that the enhancement by TRH of indomethacin‐induced gastric lesions is due to a combination of the central and peripheral actions of the ulcerogenic agents.