Browse by author
Lookup NU author(s): Viktoria Venglovecz, Dr Zoltan Rakonczay, Dr Michael Gray
Full text for this publication is not currently held within this repository. Alternative links are provided below where available.
Pancreatic ductal epithelial cells play a fundamental role in HCO3 (-) secretion, a process which is essential for maintaining the integrity of the pancreas. Although several studies have implicated impaired HCO3 (-) and fluid secretion as a triggering factor in the development of pancreatitis, the mechanism and regulation of HCO3 (-) secretion is still not completely understood. To date, most studies on the ion transporters that orchestrate ductal HCO3 (-) secretion have focussed on the role of Cl-/HCO3 (-) exchangers and Cl- channels, whereas much less is known about the role of K+ channels. However, there is growing evidence that many types of K+ channels are present in ductal cells where they have an essential role in establishing and maintaining the electrochemical driving force for anion secretion. For this reason, strategies that increase K+ channel function may help to restore impaired HCO3 (-) and fluid secretion, such as in pancreatitis, and therefore provide novel directions for future pancreatic therapy. In this review, our aims are to summarize the types of K+ channels found in pancreatic ductal cells and to discuss their individual roles in ductal HCO3 (-) secretion. We will also describe how K+ channels are involved in pathophysiological conditions and discuss how they could act as new molecular targets for the development of therapeutic approaches to treat pancreatic diseases.
Author(s): Venglovecz V, Rakonczay Z, Gray MA, Hegyi P
Publication type: Review
Publication status: Published
Journal: Pflügers Archiv - European Journal of Physiology
Year: 2015
Volume: 467
Issue: 4
Pages: 625-640
Print publication date: 01/04/2015
Online publication date: 31/07/2014
Acceptance date: 18/07/2014
ISSN (print): 0031-6768
ISSN (electronic): 1432-2013
Publisher: SPRINGER
URL: http://dx.doi.org/10.1007/s00424-014-1585-0
DOI: 10.1007/s00424-014-1585-0