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Am J Physiol Cell Physiol 276: C16-C25, 1999;
0363-6143/99 $5.00
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Vol. 276, Issue 1, C16-C25, January 1999

CFTR drives Na+-nHCOminus 3 cotransport in pancreatic duct cells: a basis for defective HCOminus 3 secretion in CF

Holli Shumaker1, Hassane Amlal1, Raymond Frizzell2, Charles D. Ulrich II3, and Manoocher Soleimani1

Divisions of 1 Nephrology and Hypertension and 3 Digestive Diseases, Department of Internal Medicine, University of Cincinnati, Cincinnati, Ohio 45267-0585; and 2 Department of Cell Biology and Physiology, University of Pittsburgh, Pittsburgh, Pennsylvania 15261

Pancreatic dysfunction in patients with cystic fibrosis (CF) is felt to result primarily from impairment of ductal HCO-3 secretion. We provide molecular evidence for the expression of NBC-1, an electrogenic Na+-HCO-3 cotransporter (NBC) in cultured human pancreatic duct cells exhibiting physiological features prototypical of CF duct fragments (CFPAC-1 cells) or normal duct fragments [CAPAN-1 cells and CFPAC-1 cells transfected with wild-type CF transmembrane conductance regulator (CFTR)]. We further demonstrate that 1) HCO-3 uptake across the basolateral membranes of pancreatic duct cells is mediated via NBC and 2) cAMP potentiates NBC activity through activation of CFTR-mediated Cl- secretion. We propose that the defect in agonist-stimulated ductal HCO-3 secretion in patients with CF is predominantly due to decreased NBC-driven HCO-3 entry at the basolateral membrane, secondary to the lack of sufficient electrogenic driving force in the absence of functional CFTR.

cystic fibrosis; cystic fibrosis transmembrane conductance regulator; electrogenic sodium-bicarbonate cotransporter; pancreatic dysfunction


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