ABSORPTION AND SECRETION IN THE COLON

Secretory diarrhea can be elicited by bacterial toxins, hormones, chem ical stimulants such as laxatives, and mediators released during mucos al inflammation. These peptide and nonpeptide mediators can have direc t and indirect effects as secretagogues by interfering with ion transp ort through channels and exchangers. Molecular biology techniques have led to the cloning of isoforms of the Na+/H+ exchanger, provided furt her information on regulation by the cystic fibrosis transmembrane con ductance regulator of Cl- channels, and identified further characteris tics of the P-type ATPase that may play a role in K+ absorption by the colon. New studies have shown that HCO-(3) secretion is stimulated by cyclic AMP and cyclic GMP. Guanylin has been found in intestinal ente rochromaffin cells, leading to speculation that it may be released lum inally from these cells. Enteric neurons and mediators produced by imm unocytes and mast cells are stimulants of secretion in inflammatory bo wel disease. In this regard, nitric oxide has variable effects on ion transport, including stimulation secretion by the rat colon and guinea pig small intestine. This free radical seems to be involved in secret ion evoked by castor oil and other laxatives. New approaches to pharma cotherapy for secretory diarrhea include studies on the enkephalinase inhibitor acetorphan, loperamide oxide, and use of the synthetic somat ostatin analogue octreotide for AIDS-related diarrhea. Glutamine was f ound more effective than glucose at stimulating Na+ absorption by the pig intestine, suggesting that it may be a useful addition to oral reh ydration solutions. The new knowledge about mechanisms of anion secret ion, mediators of secretion, and molecular mechanisms for inhibition o f secretion will undoubtedly contribute to better management of secret ory diarrhea due to enteric infection, inflammatory bowel disease, and AIDS.