Endogenous prostaglandins in gastric alkaline response in the rat stomach after damage

Abstract

A role of endogenous prostaglandins in gastric alkaline response (an increase of luminal pH) and functional recovery was investigated in the rat stomach after damage with acidified taurocholate (TC, 20 mM) or aspirin (ASA, 40 mM). Exposure of the stomach to TC or ASA similarly produced a transmucosal potential difference (PD) reduction and enhancement of H+ backdiffusion. The PD was restored gradually with time, and this process was much faster in the case of TC compared with ASA. After exposure to TC, acid secretion ceased and bicarbonate (0.5-1 mu eq/10 min) appeared in the lumen, whereas acid secretion persisted in the stomach exposed to ASA. However, in the presence of cimetidine (8 mg . kg-1 . h-1), these two agents produced a similar degree of luminal alkalinization (approximately 1 mu eq/10 min of HCO3-). Pretreatment with indomethacin (5 mg/kg, sc) significantly inhibited luminal alkalinization and PD recovery seen after exposure to TC. Concurrent administration of 16,16-dimethyl prostaglandin E2 (3 micrograms/kg, sc) antagonized the effects of indomethacin in stomachs exposed to TC and also unmasked luminal alkalinization and expedited the PD recovery in stomachs exposed to ASA. The levels of PGE2 and 6-keto-PGF1 alpha in the corpus mucosa were significantly increased in stomachs exposed to TC, but decreased in those exposed to ASA. These results indicate that luminal alkalinization of the stomach after damage with TC results from both an inhibition of acid secretion caused by endogenous prostaglandins and an increased appearance of HCO-3, and may play a role in functional recovery of the damaged mucosa. Gastric alkalinization seems to be a common phenomenon after exposure to mucosal damaging agents unless they have an inhibitory effect on prostaglandin biosynthesis.

Cytoprotective Action of L-Arginine against HCl-Induced Gastric Injury in Rats: Involvement of Nitric Oxide?

“…The involvement of endogenous PGs in the mucosal protection and the functional responses induced by mild irritants has been well-demonstrated by many investiga tors (11,(15)(16)(17). The increase of luminal pH in the stomach exposed to mild irritants is considered to be due to both inhibition of acid secretion and diffusion of HC03 (17), while the GMBF response may be mediated by endogenous PGs and capsaicin-sensitive sensory neu rons (11,18).…”

Lipid Classes, Fatty Acid Composition, and Glycerolipid Molecular Species of the Red Alga <i>Gracilaria vermiculophylla</i>, a Prostaglandin-Producing Seaweed

“…Prostaglandins are important compounds that are widely used in the pharmaceutical field because they inhibit platelet aggregation 9 , and have oxytocic 10 and gastric antisecretory actions 11 . G. vermiculophylla is a promising source of naturally occurring prostaglandins 4,12 .…”

Cytoprotective action of histamine against 0.6N HCl-induced gastric mucosal injury in rats; Comparative study with adaptive cytoprotection induced by exogenous acid.

“…We previously reported that mild irritants produced both PD reduction and increase of pH of the rat stomach and suggested a causal relationship between these changes and adaptive cytoprotection induced by mild irritants (8)(9)(10). Thus, determination of gastric PD and pH may give some information about the involvement of adaptive cytopro tection in the mechanism of mucosal pro tection afforded by gastric secretagogues.…”