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Motility‐induced but not vasoactive intestinal peptide‐induced increase in luminal alkalinization in rat duodenum is dependent on luminal Cl −
Author(s) -
Pihl L.,
Sjöblom M.,
Seidler U.,
Sedin J.,
Nylander O.
Publication year - 2010
Publication title -
acta physiologica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.591
H-Index - 116
eISSN - 1748-1716
pISSN - 1748-1708
DOI - 10.1111/j.1748-1716.2010.02112.x
Subject(s) - motility , vasoactive intestinal peptide , duodenum , medicine , stimulation , secretion , endocrinology , chemistry , extracellular , in vivo , biology , neuropeptide , biochemistry , microbiology and biotechnology , receptor
Aim: To investigate whether the motility‐ and the vasoactive intestinal peptide (VIP)‐induced increase in luminal alkalinization in the duodenum is dependent on luminal Cl − . Methods: 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. Results: 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. Conclusions: 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.