Abstract
In many species the pancreatic duct epithelium secretes HCO 3- ions at a concentration of around 140 mM by a mechanism that is only partially understood. We know that HCO3- uptake at the basolateral membrane is achieved by Na+-HCO 3- cotransport and also by a H+-ATPase and Na+/H+ exchanger operating together with carbonic anhydrase. At the apical membrane, the secretion of moderate concentrations of HCO3- can be explained by the parallel activity of a Cl-/HCO3- exchanger and a Cl- conductance, either the cystic fibrosis transmembrane conductance regulator (CFTR) or a Ca2+-activated Cl- channel (CaCC). However, the sustained secretion of HCO3- into a HCO 3--rich luminal fluid cannot be explained by conventional Cl-/HCO3- exchange. HCO3- efflux across the apical membrane is an electrogenic process that is facilitated by the depletion of intracellular Cl-, but it remains to be seen whether it is mediated predominantly by CFTR or by an electrogenic SLC26 anion exchanger. Copyright © 2005 by Annual Reviews. All rights reserved.
| Original language | English |
|---|---|
| Pages (from-to) | 377-409 |
| Number of pages | 32 |
| Journal | Annual Review of Physiology |
| Volume | 67 |
| DOIs | |
| Publication status | Published - 2005 |
UN SDGs
This output contributes to the following UN Sustainable Development Goals (SDGs)
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SDG 3 Good Health and Well-being
Keywords
- Carbonic anhydrase
- CFTR
- Epithelial transport
- Intracellular pH
- Secretin
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