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Ca2+-activated K+ currents of pancreatic duct cells in guinea-pig

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Authors

Lee, Han-Wook; Li, Jingchao; Koo, Na-Youn; Piao, Zheng Gen; Hwang, Sung Min; Han, Jae-Woong; Lee, Jong-Heun; Choi, Han-Saem; Kim, Joong Soo; Park, Kyungpyo

Issue Date
2004-12
Publisher
대한생리약리학회
Citation
Korean J Physiol Pharmacol 8: 335-338
Keywords
Duct cellsGuinea pigPancreasK+ currentsCa2+
Abstract
There are numerous studies on transepithelial transports in duct cells including Cl- and/or HCO3-. However, studies on transepithelial K+ transport of normal duct cells in exocrine glands are scarce. In the present study, we examined the characteristics of K+ currents in single duct cells isolated from guinea pig pancreas, using a whole-cell patch clamp technique. Both Cl- and K+ conductance were found with KCl rich pipette solutions. When the bath solution was changed to low Cl-, reversal potentials shifted to the negative side, -75±4 mV, suggesting that this current is dominantly selective to K+. We then characterized this outward rectifying K+ current and examined its Ca22+ dependency. The K+ currents were activated by intracellular Ca22+. 100 nM or 500 nM Ca22+ in pipette significantly (P<0.05) increased outward currents (currents were normalized, 76.8?7.9 pA, n=4 or 107.9?35.5 pA, n=6) at +100 mV membrane potential, compared to those with 0 nM Ca2+ in pipette (27.8?3.7 pA, n=6). We next examined whether this K+ current, recorded with 100 nM Ca2+ in pipette, was inhibited by various inhibitors, including Ba2+, TEA and iberiotoxin. The currents were inhibited by 40.4±% (n=3), 87.0±% (n=5) and 82.5±% (n=9) by 1 mM Ba2+, 5 mM TEA and 100 nM iberiotoxin, respectively. Particularly, an almost complete inhibition of the current by 100 nM iberiotoxin further confirmed that this current was activated by intracellular Ca2+. The K+ current may play a role in secretory process, since recycling of K+ is critical for the initiation and sustaining of Cl- or HCO32+ secretion in these cells.
ISSN
1226-4512
Language
English
URI
https://hdl.handle.net/10371/66604
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