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MEMBRANE TRANSPORTERS, ION CHANNELS, AND PUMPS

Substance P inhibits bicarbonate secretion from guinea pig pancreatic ducts by modulating an anion exchanger

Department of Physiological Sciences, University Medical School, Newcastle upon Tyne NE2 4HH, United Kingdom

Submitted 9 December 2002 ; accepted in final form 13 March 2003

The stimulatory pathways controlling HCO₃^- secretion by the pancreatic ductal epithelium are well described. However, only a few data are available concerning inhibitory mechanisms, which may play an important role in the physiological control of the pancreas. The aim of this study was to investigate the cellular mechanism by which substance P (SP) inhibits pancreatic ductal HCO₃^- secretion. Small intra/interlobular ducts were isolated from the pancreas of guinea pigs. During overnight culture the ducts seal to form a closed sac. Transmembrane HCO₃^- fluxes were calculated from changes in intracellular pH (measured using the pH-sensitive dye BCECF) and the buffering capacity of the cells. We found that secretin can stimulate HCO₃^- secretion in guinea pig pancreatic ducts about fivefold and that this effect could be totally blocked by SP. The inhibitory effect of SP was relieved by spantide, an SP receptor antagonist. SP had no effect on the activity of basolateral Na⁺-HCO₃^- cotransporters and Na⁺/H⁺ exchangers. However, the peptide did inhibit a Cl^--dependent HCO₃^- efflux (secretory) mechanism, most probably the Cl^-/HCO₃ exchanger on the apical membrane of the duct cell.

pancreas; Cl^-/HCO₃^- exchanger; tachykinin

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