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Interactive roles of endogenous prostaglandin and nitric oxide in regulation of acid secretion by damaged rat stomachs
Author(s) -
Takeuchi K.,
Sugamoto S.,
Yamamoto H.,
Kawauchi S.,
Tashima K.
Publication year - 2000
Publication title -
alimentary pharmacology and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.308
H-Index - 177
eISSN - 1365-2036
pISSN - 0269-2813
DOI - 10.1046/j.1365-2036.2000.014s1125.x
Subject(s) - endogeny , nitric oxide , secretion , medicine , prostaglandin , endocrinology , pharmacology , biochemistry , biology
Summary Background : The acid inhibitory mechanism in the damaged stomach is known to involve endogenous nitric oxide (NO) as well as prostaglandin (PG). Aim : To investigate the interaction between PG and NO in regulation of acid secretion in the stomach following damage. Methods : Under urethane anaesthesia, a rat stomach was mounted in an ex vivo chamber and perfused with saline. Acid secretion, luminal PGE 2 , NO metabolites (NO x ) and histamine output were measured before and after application of 20 m m taurocholate Na (TC) for 30 min, with or without pre‐treatment with indomethacin and/or N G ‐nitro‐ l ‐arginine methyl ester (L‐NAME). Results : Exposure of the stomach to TC caused a decrease in acid secretion, with concomitant increase of both luminal NO x and PGE 2 . Either L‐NAME or indomethacin reduced the decrease in acid secretion in response to TC, but only L‐NAME allowed acid secretion to increase over basal values. L‐NAME prevented the increase of luminal NO x after TC treatment, while indomethacin inhibited PGE 2 release during and after exposure to TC. The increase in acid secretion in the presence of L‐NAME was prevented when indomethacin was given concomitantly. TC treatment increased histamine output in the lumen, a process that was enhanced by L‐NAME but reduced by indomethacin. Conclusions : Damage to the stomach increases both NO and PG in the lumen, and decreases acid secretion. Inhibiting NO production increases acid secretion in the damaged stomach, but only when PG biosynthesis is intact. It is assumed that endogenous PG has a dual role in the regulation of acid secretion in the damaged stomach: an inhibitory effect at the parietal cell and an excitatory effect probably through enhancing the release of mucosal histamine.