Abstract
THE molecular mechanism by which cholera toxin produces a massive loss of water and electrolytes is unknown, but it is clear that an increase in net secretion of approximately isotonic fluid occurs throughout the length of the small intestine1,2. The relative contributions of increased active ion secretion and decreased active ion reabsorption to this fluid production are also unknown, although the fluid contains more HCO−3 than does plasma1,3. The toxin might stimulate secretory transport processes, for example Cl− and HCO−3, to such an extent that reabsorptive capacity is exceeded, water is held osmotically and massive diarrhoea results.
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