K+ channels on resting duct cells from rat pancreas

• Material Type: 文書・図像類
• Title: K+ channels on resting duct cells from rat pancreas
• Author/Editor: Hayashi, Mikio; Matsuda, Hiroko
• Author Heading: Hayashi, Mikio; Matsuda, Hiroko
• Publication, Distribution, etc.: Faculty of Medicine Tokushima University
• Publication Date: 2009-12
• Publication Date (W3CDTF): 2009-12
• Periodical title: The Journal of Medical Investigation
• No. or year of volume/issue: 56 Supplement
• Volume: 56
• Issue: Supplement
• Pages: 354-354
• ISSN (Periodical Title): ISSN : 1349-6867; ISSN : 1343-1420
• Text Language Code: eng
• Subject Heading: pancreatic duct; potassium channel; patch clamp
• Target Audience: 一般
• Note (General): The ductal system of the exocrine pancreas produces HCO3--rich fluid in response to secretin and other stimuli. HCO3- efflux across the luminal membrane is mediated by a Cl--HCO3- exchanger operating in parallel with the cystic fibrosis transmembrane conductance regulator (CFTR) Cl- channel. Basolateral K+ channels provide an exit pathway for K+ and play a vital role in maintaining the membrane potential, which is a crucial component of the driving force for anion secretion. Measurements of membrane potential with intracellular microelectrodes suggested that Ba2+-sensitive K+ conductance accounts for more than 60% of the total basolateral ionic conductance in resting ducts (1). To identify the Ba2+-sensitive K+ channels, we isolated ducts from normal rat pancreas by collagenase digestion. We first demonstrated that the ducts did not express a vascular endothelial marker PECAM-1 (platelet/endothelial cell adhesion molecule-1), but expressed cytokeratin 20, a marker of duct cells (2), using immunofluorescent staining. In addition, monoclonal anti-CFTR antibody was detected near the luminal membrane of these cells. In cell-attached single-channel recordings, we observed three types of K+ channels on basolateral membrane in unstimulated duct cells. The 40 pS K+ channels are likely to mediate whole-cell inwardly rectifying K+ (Kir) currents, which were blocked by extracellular Ba2+ in a voltage-dependent manner. The properties of 90 pS and 170 pS K+ channels are similar to those of Ca2+-activated K+ channels. We then identified Kir2.0 and SK4/IK1 (intermediate conductance Ca2+-activated K+ channel) subunits as molecular candidates of the K+ channels using RT-PCR analysis. The present results suggest that these subunits may mediate native K+ currents in resting duct cells. Further functional studies with specific blockers are required to evaluate which of these K+ channels contribute to the resting membrane potential and might be involved in HCO3- secretion.
• Access Restrictions: 限定公開
• Related Material (DOI): 10.2152/jmi.56.354
• Periodical Title (NCID): AA11166929; https://ci.nii.ac.jp/ncid/AA11166929; AA12022913; https://ci.nii.ac.jp/ncid/AA12022913
• Data Provider (Database): 国立情報学研究所 : 学術機関リポジトリデータベース（IRDB）（機関リポジトリ）; https://irdb.nii.ac.jp
• Original Data Provider (Database): 徳島大学 : 徳島大学機関リポジトリ