MECHANISMS OF BICARBONATE SECRETION IN THE PANCREATIC DUCT

  • Martin C. Steward
    Faculty of Life Sciences, University of Manchester, Manchester M13 9PT, United Kingdom;
  • Hiroshi Ishiguro
    Human Nutrition and Internal Medicine, Nagoya University Graduate School of Medicine, Nagoya 464-8601, Japan;
  • R. Maynard Case
    Faculty of Life Sciences, University of Manchester, Manchester M13 9PT, United Kingdom;

抄録

<jats:p> ▪ Abstract  In many species the pancreatic duct epithelium secretes HCO<jats:sub>3</jats:sub><jats:sup>−</jats:sup> ions at a concentration of around 140 mM by a mechanism that is only partially understood. We know that HCO<jats:sub>3</jats:sub><jats:sup>−</jats:sup> uptake at the basolateral membrane is achieved by Na<jats:sup>+</jats:sup>-HCO<jats:sub>3</jats:sub><jats:sup>−</jats:sup> cotransport and also by a H<jats:sup>+</jats:sup>-ATPase and Na<jats:sup>+</jats:sup>/H<jats:sup>+</jats:sup> exchanger operating together with carbonic anhydrase. At the apical membrane, the secretion of moderate concentrations of HCO<jats:sub>3</jats:sub><jats:sup>−</jats:sup> can be explained by the parallel activity of a Cl<jats:sup>−</jats:sup>/HCO<jats:sub>3</jats:sub><jats:sup>−</jats:sup> exchanger and a Cl<jats:sup>−</jats:sup> conductance, either the cystic fibrosis transmembrane conductance regulator (CFTR) or a Ca<jats:sup>2+</jats:sup>-activated Cl<jats:sup>−</jats:sup> channel (CaCC). However, the sustained secretion of HCO<jats:sub>3</jats:sub><jats:sup>−</jats:sup> into a HCO<jats:sub>3</jats:sub><jats:sup>−</jats:sup>-rich luminal fluid cannot be explained by conventional Cl<jats:sup>−</jats:sup>/HCO<jats:sub>3</jats:sub><jats:sup>−</jats:sup> exchange. HCO<jats:sub>3</jats:sub><jats:sup>−</jats:sup> efflux across the apical membrane is an electrogenic process that is facilitated by the depletion of intracellular Cl<jats:sup>−</jats:sup>, but it remains to be seen whether it is mediated predominantly by CFTR or by an electrogenic SLC26 anion exchanger. </jats:p>

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