{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,4]],"date-time":"2026-10-04T08:34:03Z","timestamp":1791102843806,"version":"4.1.0"},"reference-count":46,"publisher":"Rockefeller University Press","issue":"3","content-domain":{"domain":["rupress.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2009,3,1]]},"abstract":"<jats:p>Pancreatic duct epithelium secretes a HCO3\u2212-rich fluid by a mechanism dependent on cystic fibrosis transmembrane conductance regulator (CFTR) in the apical membrane. However, the exact role of CFTR remains unclear. One possibility is that the HCO3\u2212 permeability of CFTR provides a pathway for apical HCO3\u2212 efflux during maximal secretion. We have therefore attempted to measure electrodiffusive fluxes of HCO3\u2212 induced by changes in membrane potential across the apical membrane of interlobular ducts isolated from the guinea pig pancreas. This was done by recording the changes in intracellular pH (pHi) that occurred in luminally perfused ducts when membrane potential was altered by manipulation of bath K+ concentration. Apical HCO3\u2212 fluxes activated by cyclic AMP were independent of Cl\u2212 and luminal Na+, and substantially inhibited by the CFTR blocker, CFTRinh-172. Furthermore, comparable HCO3\u2212 fluxes observed in ducts isolated from wild-type mice were absent in ducts from cystic fibrosis (\u0394F) mice. To estimate the HCO3\u2212 permeability of the apical membrane under physiological conditions, guinea pig ducts were luminally perfused with a solution containing 125 mM HCO3\u2212 and 24 mM Cl\u2212 in the presence of 5% CO2. From the changes in pHi, membrane potential, and buffering capacity, the flux and electrochemical gradient of HCO3\u2212 across the apical membrane were determined and used to calculate the HCO3\u2212 permeability. Our estimate of \u223c0.1 \u00b5m sec\u22121 for the apical HCO3\u2212 permeability of guinea pig duct cells under these conditions is close to the value required to account for observed rates of HCO3\u2212 secretion. This suggests that CFTR functions as a HCO3\u2212 channel in pancreatic duct cells, and that it provides a significant pathway for HCO3\u2212 transport across the apical membrane.<\/jats:p>","DOI":"10.1085\/jgp.200810122","type":"journal-article","created":{"date-parts":[[2009,2,10]],"date-time":"2009-02-10T02:09:23Z","timestamp":1234231763000},"page":"315-326","update-policy":"https:\/\/doi.org\/10.1085\/jgp.crossmarkpolicy","source":"Crossref","is-referenced-by-count":110,"title":["CFTR Functions as a Bicarbonate Channel in Pancreatic Duct Cells"],"prefix":"10.1085","volume":"133","author":[{"given":"Hiroshi","family":"Ishiguro","sequence":"first","affiliation":[{"name":"Human Nutrition 1 and 2"},{"name":"Gastroenterology, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan 1 and 2"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Martin C.","family":"Steward","sequence":"additional","affiliation":[{"name":"Faculty of Life Sciences, University of Manchester, Manchester M13 9NT, England, UK 3"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Satoru","family":"Naruse","sequence":"additional","affiliation":[{"name":"Human Nutrition 1 and 2"},{"name":"Gastroenterology, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan 1 and 2"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shigeru B.H.","family":"Ko","sequence":"additional","affiliation":[{"name":"Human Nutrition 1 and 2"},{"name":"Gastroenterology, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan 1 and 2"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hidemi","family":"Goto","sequence":"additional","affiliation":[{"name":"Human Nutrition 1 and 2"},{"name":"Gastroenterology, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan 1 and 2"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"R. 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