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Anion interactions with CFTR and consequences for HCO3- transport in secretory epithelia

Lookup NU author(s): Dr Michael Gray, Dr Catherine O'Reilly, Dr John Winpenny, Professor Barry Argent


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We have been studying CFTR channels in guinea pig pancreatic duct cells and rather surprisingly found that luminal HCO3- had a pronounced inhibitory effect on cAMP-activated CFTR chloride currents. The block produced by HCO3- was rapid, voltage-independent and occurred over a physiological range of extracellular HCO3- concentrations. I- and ClO4- were also found to inhibit CFTR currents, but both were less effective than HCO3-. Although we have not identified how HCO3- is able to block CFTR our data suggests that an external anion-binding site on the channel itself is involved. Overall, our results show that luminal HCO3- acts as a potent inhibitor of CFTR channels (and by inference CFTR-mediated secretion), under normal physiological conditions. These data have implications not only for current models of pancreatic duct cell HCO3- transport, but also for other bicarbonate-secreting tissues, such as the liver, GI tract and lungs.

Publication metadata

Author(s): Gray M, O'Reilly C, Winpenny J, Argent B

Publication type: Article

Publication status: Published

Journal: Journal of Korean Medical Science

Year: 2000

Volume: 15

Pages: S12-S15

ISSN (print): 1011-8934

ISSN (electronic): 1598-6357

Publisher: Korean Academy of Medical Sciences