Abstract
Current information is reviewed on the mechanism of secretion in small intestine, including how it is altered by cyclic 3′, 5′-adenosine monophosphate and on the structures and properties of cholera and both heat-labile and heat-stable Escherichia coli enterotoxins. Two separate active ion transport processes are altered by cyclic 3′,5′-adenosine monophosphate: 1) coupled absorption of NaCl is inhibited in villus cells and 2) active anion secretion is stimulated, probably in crypt cells. Cholera and heat-labile E. coli toxins exert their secretory effect by stimulating intestinal mucosal adenylate cyclase. This stimulation results from the A1 subunitcatalyzed transfer of adenosine diphosphate ribose from NAD to a membrane-bound guanosine triphosphatase, thereby inhibiting this enzyme, which normally represses adenylate cyclase. Heatstable E. coli enterotoxin stimulates intestinal mucosal guanylate cyclase, which appears to be the basis for its enterotoxicity.
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