| Title | Bicarbonate Transport by the Human Pancreatic Ductal Cell Line HPAF. | | Author(s) | Demeter I, Hegyesi O, Nagy AK, Case MR, Steward MC, Varga G, Burghardt B | | Institution | From the *Department of Oral Biology, Semmelweis University, Budapest, Hungary; and daggerFaculty of Life Sciences, University of Manchester, Manchester, United Kingdom. | | Source | Pancreas 2009 Sep 8. | | Abstract | OBJECTIVES:: The human pancreatic duct cell line, HPAF, has been shown previously to secrete Cl in response to Ca-mobilizing stimuli. Our aim was to assess the capacity of HPAF cells to transport and secrete HCO3.
METHODS:: HPAF cells were grown as confluent monolayers on permeable supports. Short-circuit current was measured by voltage clamp. Intracellular pH (pHi) was measured by microfluorometry in cells loaded with 2',7'-bis(2-carboxyethyl)-5(6)-carboxyfluorescein (BCECF).
RESULTS:: In HCO3-free solutions, ATP-evoked changes in short-circuit current were inhibited by bumetanide, and the recovery of pHi from acid loading was abolished by 5-(N-ethyl-N-isopropyl)-amiloride (EIPA). In the presence of HCO3, ATP-evoked secretion was no longer inhibited by bumetanide, and there was a strong EIPA-insensitive recovery from acid loading, which was inhibited by 4,4'-diisothiocyanatodihydrostilbene-2,2'-disulfonate (H2DIDS). ATP, but not forskolin, stimulated HCO3 efflux from the cells.
CONCLUSIONS:: In the absence of HCO3, ATP-evoked Cl secretion is driven by a basolateral Na-K-2Cl cotransporter, and pHi is regulated by apical and basolateral Na/H exchangers. In the presence of HCO3, ATP-evoked secretion is sustained in the absence of Na-K-2Cl cotransporter activity and is probably driven by basolateral Na-HCO3 cotransport. | | Language | ENG | | Pub Type(s) | JOURNAL ARTICLE
| | PubMed ID | 19745779 |
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