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REGULATION OF ION TRANSPORT BY 5-HYDROXYTRYPTAMINE IN RAT COLON

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SUMMARY

1. 5-Hydroxytryptamine (5-HT) modulates the motility and secretion of the gastrointestinal tract. To examine the direct effect of 5-HT on the secretions of colonic epithelial cells, a short-circuit current was used to measure electrolyte transport in the rat stripped distal colon. A neuronal Na+ channel blocker and a cyclo-oxygenase inhibitor were routinely added in experiments to abolish the effects of the enteric nervous system and endogenous prostaglandin, respectively.

2. Basolateral application of 5-HT (10 µmol/L) induced an increase in the short circuit current (ISC). Removal of extracellular Cl, HCO3 or both resulted in a 59.6, 76.4 and 90% reduction of 5-HT-elicited responses, respectively. The Ca2+-dependent Cl channel blocker 4,4′-diisothiocyanatostilbene-2,2′-disulphonic acid (DIDS) had no effect on the 5-HT-induced increase in ISC, but the selective cystic fibrosis transmembrane conductance regulator (CFTR) channel blocker glibenclamide (1 mmol/L) inhibited 5-HT-induced increases in ISC by approximately 92.9%. Removal of apical Na+ reduced the 5-HT-induced increase in ISC by 33.3%.

3. Basolateral pretreatment with 100 µmol/L bumetanide (an inhibitor of the Na+–K+−2Cl cotransporter), 200 µmol/L DIDS (an inhibitor of the Na+–HCO3 transporter or the Cl/HCO3 exchanger) or both decreased the ΔISC induced by 5-HT by approximately 75.5, 59.0 and 86.3%, respectively. Removal of basolateral Na+ also reduced the current evoked by 5-HT.

4. The selective 5-HT4 antagonist GR113808 (1 µmol/L) totally abolished the 5-HT-induced increase in ISC, whereas 2-methyl-5-HT (100 µmol/L) induced a weak ISC response.

5. In conclusion, the present study has demonstrated that 5-HT can elicit Cl- and HCO3 anion secretion and Na+ absorption by acting directly on colonic epithelial cells via 5-HT4 receptors.
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Keywords: 5-HT4 receptor; 5-hydroxytryptamine; colon; ion secretion; short-circuit current

Document Type: Research Article

Affiliations: Epithelial Cell Biology Research Center, Department of Physiology, Faculty of Medicine, The Chinese University of Hong Kong, Shatin, Hong Kong and

Publication date: July 1, 2004

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