Stimulation of HCO3- secretion across cystic fibrosis pancreatic duct cells by extracellular ATP

Biol Signals Recept. 1998 Nov-Dec;7(6):321-7. doi: 10.1159/000014555.

Abstract

Previous studies have demonstrated that extracellular ATP is able to activate Ca2+-dependent Cl- channels which may be important in circumventing the defective cAMP-dependent pancreatic ductal HCO3- secretion in cystic fibrosis (CF). The present study further investigated the effect of extracellular ATP on the stimulation of HCO3- secretion across CF pancreatic duct cells (CFPAC-1). Cells were grown in culture plate inserts which enabled the access of a pH microelectrode to the apical compartment. Changes in apical pH upon stimulation by extracellular ATP, as an indication of HCO3- secretion, were measured. ATP induced a rapid increase in apical pH, which reached a plateau with an averaged pH unit of 0.3 higher than that measured in unstimulated cells. The effect of ATP was concentration dependent. The ATP-induced change in pH could be blocked by apical addition of Cl- channel blockers, indicating that activation of apical Cl- channel is vital for HCO3- secretion by the pancreatic duct cells. Together with the previous finding, the present study suggests that HCO3- secretion may be stimulated in CF pancreatic duct cells by extracellular ATP via a cAMP-independent pathway.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenosine Triphosphate / administration & dosage
  • Adenosine Triphosphate / pharmacology*
  • Bicarbonates / metabolism*
  • Cells, Cultured
  • Chloride Channels / antagonists & inhibitors
  • Cystic Fibrosis / metabolism*
  • Humans
  • Hydrogen-Ion Concentration
  • Ion Transport / drug effects
  • Pancreatic Ducts / drug effects*
  • Pancreatic Ducts / metabolism*
  • ortho-Aminobenzoates / pharmacology

Substances

  • Bicarbonates
  • Chloride Channels
  • ortho-Aminobenzoates
  • Adenosine Triphosphate
  • fenamic acid