Implications of gastric topical bioactive peptides in ammonia-induced acute gastric mucosal lesions in rats.

Abstract:

BACKGROUND:Ammonia, one of the pathogenic factors in Helicobacter pylori-induced mucosal injury, induces acute mucosal lesions in the rat glandular stomach. METHODS:The effect of ammonia administered intragastrically on gastric peptides was investigated in urethane-anesthetized rats. RESULTS:Gastric mucosal lesions were observed 5 min after 0.3% ammonia (4 ml/kg, intragastrically). Immunoreactive endothelin-1 (ET-1) and immunoreactive thyrotropin-releasing hormone (TRH) concentrations in the gastric wall decreased significantly 2 min and 5 min after ammonia, respectively. A significant increase in gastric juice immunoreactive ET-1 and TRH levels was reciprocally observed. The severity of gastric mucosal injury and changes in gastric immunoreactive ET-1 and TRH concentrations were shown to be concentration-dependent 30 min after ammonia. Atropine (5 mg/kg, intraperitoneally, -20 min) prevented ammonia-induced injury accompanied by a block of changes in gastric immunoreactive ET-1 and TRH concentrations. BQ-485 (ET(A) receptor antagonist; 2 mg/kg, subcutaneously) also abolished ammonia-induced lesions and gastric immunoreactive TRH changes. CONCLUSIONS:These findings suggested that gastric ET-1 and TRH play a role in ammonia-induced gastric mucosal injury mediated via a muscarine and an ET(A) receptor.

journal_name

Scand J Gastroenterol

authors

Mori S,Kaneko H,Mitsuma T,Hayakawa T,Yamaguchi C,Uruma M

doi

10.1080/00365529850171017

subject

Has Abstract

pub_date

1998-04-01 00:00:00

pages

386-93

issue

4

eissn

0036-5521

issn

1502-7708

journal_volume

33

pub_type

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