PGE2 stimulates gastric chloride transport: possible key to cytoprotection

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Abstract
Prostaglandins protect the stomach against a variety of noxious agents independently of effects on acid secretion, but the mechanism of this 'cytoprotection' is unknown. We recently proposed that gastric surface cells extrude or eliminate luminal acid by a process analogous to that described in squid axon, snail neurone, and barnacle muscle. Influxing luminal H+ combines with HCO3- which has entered the cell in exchange for intracellular chloride, probably at the nutrient membrane. Dehydration of the resulting H2CO3 into CO2 and H2O is catalysed by carbonic anhydrase, which is present in surface cells in large amounts. Interference with this chain of reactions at any point frequently causes ulceration. We have examined the effect of 16,16-dimethylprostaglandin E2 (PGE) on different segments of this protective mechanism and show here that the protective effects are intimately associated with stimulation of chloride transport. All experiments were done in vitro thus eliminating any effects of prostaglandin on mucosal circulation.