Fig. 5.

Ion transport in acinar (a) and pancreatic duct cells (b). a Upon stimulation with acetylcholine, cholecystokinin or other agonists, intracellular [Ca²⁺] increases and stimulates NaCl and fluid secretion, as well as the exocytosis of enzyme-containing secretory granules. As these granules also contain H⁺, the local pH falls to approximately 6.8. Cl⁻ secretion occurs through a CaCC on the apical membrane. b CFTR conducts Cl⁻ and HCO₃ ⁻ and works in concert with a Cl⁻/HCO₃ ⁻ apical exchanger, to mediate net transepithelial HCO₃ ⁻ secretion, with Cl⁻ recycling across the apical membrane. Na⁺ moves paracellularly in response to transepithelial HCO₃ ⁻ secretion, and water follows osmotically, to produce a HCO₃ ⁻-rich isotonic fluid. Cl⁻ accumulates across the basolateral membrane via NKCC1 and accumulation of HCO₃ ⁻ inside the cells occurs through the hydration of CO₂ to HCO₃ ⁻ and H⁺ by carbonic anhydrase (CA), together with backward transport of H⁺ via the basolateral Na⁺/H exchanger (NHE). This is driven by the Na⁺ gradient established by the Na⁺/K⁺-ATPase. The Na⁺-Bicarbonate cotransporter (NBC) helps accumulate HCO₃ ⁻ within the cell and maintain an electrical driving force for efflux of HCO₃ ⁻ across the apical membrane. It also works with K⁺ channels to maintain a negative membrane potential