Abstract
THERE is considerable evidence that cholera diarrhoea is caused by accumulation of cyclic AMP in intestinal mucosa, stimulated by cholera enterotoxin1–3. Prostaglandin-E1 (PGE1) reproduces the effects of cholera enterotoxin on both cyclic AMP and secretion of fluid and electrolytes by intestinal mucosa3 and it was suggested4 that the toxin might first act by stimulating the release or synthesis of prostaglandin which then acts through cyclic AMP. Bennett4 proposed that acidic anti-inflammatory drugs, as they are potent inhibitors of prostaglandin synthesis in several tissues5–7, might antagonize the effect of cholera enterotoxin. Jacoby and Marshall reported that indomethacin, aspirin, and several other anti-inflammatory agents inhibited the cholera toxin-induced accumulation of fluid in ileal-ligated rats8. Because of its potential therapeutic significance, I have studied this proposed mechanism.
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BOURNE, H. Cholera Enterotoxin: Failure of Anti-inflammatory Agents to Prevent Cyclic AMP Accumulation. Nature 241, 399 (1973). https://doi.org/10.1038/241399a0
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DOI: https://doi.org/10.1038/241399a0
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