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PGE2 stimulates gastric chloride transport: possible key to cytoprotection

Nature volume 283, pages 671–673 (1980)Cite this article

Abstract

Prostaglandins protect the stomach against a variety of noxious agents independently of effects on acid secretion, but the mechanism of this ‘cytoprotection’ is unknown1. We recently proposed2 that gastric surface cells extrude or eliminate luminal acid by a process analogous to that described in squid axon3, snail neurone4, and barnacle muscle5. Influxing luminal H+ combines with HCO−3 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 amounts6. Interference with this chain of reactions at any point frequently causes ulceration2. 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.

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Authors and Affiliations

  1. Departments of Surgery, Harvard Medical School, Beth Israel Hospital, 330 Brookline Avenue, Boston, Massachusetts, 02215

    Rudolf Schiessel, Jeffrey Matthews, Ami Barzilai, Aryeh Merhav & William Silen

Authors
  1. Rudolf Schiessel
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  2. Jeffrey Matthews
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  3. Ami Barzilai
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  4. Aryeh Merhav
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  5. William Silen
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Schiessel, R., Matthews, J., Barzilai, A. et al. PGE2 stimulates gastric chloride transport: possible key to cytoprotection. Nature 283, 671–673 (1980). https://doi.org/10.1038/283671a0

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