Abstract
Background: Exposure of the pancreas to bile acids is considered to be one of the possible causes of acute pancreatitis, although the precise cellular mechanism underlying the bile-induced pancreatitis is still not clear. Our group has previously shown that luminal administration of chenodeoxycholate (CDC) at a low concentration (100µM) stimulated HCO3- secretion in intact guinea pig pancreatic ducts (Venglovecz et al., Gut 2008). Our preliminary experiments suggested that bile acids stimulate a calcium-dependent K+ channel in pancreatic ductal epithelial cells (PDEC), therefore, the aim of this study was to investigate the role of K+ channels in the CDC-stimulated pancreatic ductal bicarbonate secretion.
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