ArticleThe Journal of general physiology2002
Membrane potential and bicarbonate secretion in isolated interlobular ducts from guinea-pig pancreas.
Article in The Journal of general physiology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 59 citations in OpenAlex.
- Cystic Fibrosis of the Pancreas: In Vitro Duct Models for CFTR-Targeted Translational Research.International journal of molecular sciences · 2026Review
- Bicarbonate-rich fluid secretion predicted by a computational model of guinea-pig pancreatic duct epithelium.The Journal of physiology · 2017Article
- Role of CFTR in epithelial physiology.Cellular and molecular life sciences : CMLS · 2017Review
- Deletion of Slc26a6 alters the stoichiometry of apical Cl-/HCO-3 exchange in mouse pancreatic duct.American journal of physiology. Cell physiology · 2012Article
- Physiology and pathophysiology of bicarbonate secretion by pancreatic duct epithelium.Nagoya journal of medical science · 2012Review
- Molecular mechanism of pancreatic and salivary gland fluid and HCO3 secretion.Physiological reviews · 2012Review
- Trypsin reduces pancreatic ductal bicarbonate secretion by inhibiting CFTR Cl⁻ channels and luminal anion exchangers.Gastroenterology · 2011Article
- Functional coupling of apical Cl-/HCO3- exchange with CFTR in stimulated HCO3- secretion by guinea pig interlobular pancreatic duct.American journal of physiology. Gastrointestinal and liver physiology · 2009Article
- CFTR functions as a bicarbonate channel in pancreatic duct cells.The Journal of general physiology · 2009Article
- Pancreatic duct secretion: experimental methods, ion transport mechanisms and regulation.Journal of physiology and biochemistry · 2008Review
- Characterization of H+ and HCO3- transporters in CFPAC-1 human pancreatic duct cells.World journal of gastroenterology · 2006Article
- Electrophysiological characterization of native Na+-HCO3- cotransporter current in bovine parotid acinar cells.The Journal of physiology · 2005Article
- Basolateral anion transport mechanisms underlying fluid secretion by mouse, rat and guinea-pig pancreatic ducts.The Journal of physiology · 2004Article
- Gating of CFTR by the STAS domain of SLC26 transporters.Nature cell biology · 2004Article
- Ethanol induces fluid hypersecretion from guinea-pig pancreatic duct cells.The Journal of physiology · 2003Article
- Substance P inhibits bicarbonate secretion from guinea pig pancreatic ducts by modulating an anion exchanger.American journal of physiology. Cell physiology · 2003Article
- Molecular basis of potassium channels in pancreatic duct epithelial cells.Channels (Austin, Tex.)Review
- The SLC26 gene family of anion transporters and channels.Molecular aspects of medicineReview
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The interlobular duct cells of the guinea-pig pancreas secrete HCO(3)(-) across their luminal membrane into a HCO(3)(-)-rich (125 mM) luminal fluid against a sixfold concentration gradient. Since HCO(3)(-) transport cannot be achieved by luminal Cl-/HCO(3)(-) exchange under these conditions, we have investigated the possibility that it is mediated by an anion conductance. To determine whether the electrochemical potential gradient across the luminal membrane would favor HCO(3)(-) efflux, we have measured the intracellular potential (V(m)) in microperfused, interlobular duct segments under various physiological conditions. When the lumen was perfused with a 124 mM Cl- -25 mM HCO(3)(-) solution, a condition similar to the basal state, the resting potential was approximately -60 mV. Stimulation with dbcAMP or secretin caused a transient hyperpolarization (approximately 5 mV) due to activation of electrogenic Na+-HCO(3)(-) cotransport at the basolateral membrane. This was followed by depolarization to a steady-state value of approximately -50 mV as a result of anion efflux across the luminal membrane. Raising the luminal HCO(3)(-) concentration to 125 mM caused a hyperpolarization (approximately 10 mV) in both stimulated and unstimulated ducts. These results can be explained by a model in which the depolarizing effect of Cl- efflux across the luminal membrane is minimized by the depletion of intracellular Cl- and offset by the hyperpolarizing effects of Na+-HCO(3)(-) cotransport at the basolateral membrane. The net effect is a luminally directed electrochemical potential gradient for HCO(3)(-) that is sustained during maximal stimulation. Our calculations indicate that the electrodiffusive efflux of HCO(3)(-) to the lumen via CFTR, driven by this gradient, would be sufficient to fully account for the observed secretory flux of HCO(3)(-).
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