Motility-induced but not vasoactive intestinal peptide-induced increase in luminal alkalinization in rat duodenum is...

to investigate whether the motility- and the vasoactive intestinal peptide (VIP)-induced increase in luminal alkalinization in the duodenum is dependent on luminal Cl(-).

experiments were performed in anaesthetized rats in vivo. The proximal duodenum was perfused luminally with an isotonic solution, containing zero or low Cl(-) and the effects on luminal alkalinization, motility, fluid flux and epithelial permeability were determined. Parecoxib, a COX-2 inhibitor, was used to induce duodenal contractions.

control rats lacked duodenal wall contractions while parecoxib-treated ones exhibited contractions throughout the experiment. Most animals had a net fluid absorption during the perfusion with isotonic NaCl. Luminal alkalinization was about 100% higher in parecoxib-treated rats than in controls. Cl(-) -free solutions did not affect epithelial permeability or motility but decreased luminal alkalinization by ≥50% and decreased net fluid absorption in both control and parecoxib-treated animals. Reduction in luminal Cl(-) decreased alkalinization in a concentration-dependent manner. The parecoxib-induced increase in alkalinization was markedly reduced in the absence of luminal Cl(-) . VIP increased luminal alkalinization and induced fluid secretion. The lack of luminal Cl(-) did not affect the VIP-induced increase in alkalinization but reduced fluid secretion.

the parecoxib-induced increase in luminal alkalinization is highly dependent on luminal Cl(-) and it is proposed that COX-2 inhibition, via induction of duodenal motility, enhances HCO(3) (-) efflux through stimulation of apical Cl(-) /HCO(3) (-) exchange in duodenal epithelial cells. Although the VIP-induced stimulation of fluid secretion is partly dependent on luminal Cl(-) , the VIP-induced increase in luminal alkalinization is not.