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• W2053011890 startingPage "193" @default.
• W2053011890 abstract "The epithelial Na+ channel (ENaC) contributes to control of blood pressure by reabsorbing Na+ in the cortical collecting duct of the kidney. The luminal Cl- concentration in the duct varies under physiological conditions. As the body Na+ content is lower, the luminal Cl- concentration in the duct becomes lower. Thus, we hypothesized that the extracellular Cl- elevates ENaC activity in AVT-stimulated renal epithelial A6 cells (a model cell line of the cortical collecting duct) leading to recovery from a low body Na+ content. To clarify this point, we studied effects of extracellular Cl- concentration on ENaC activity using cell-attached patch clamp technique. We found that ENaC had a single-channel conductance of 4.6 ± 0.1 pS (mean ± SE) and channel activity (open probability, Po) of 0.30 ± 0.02 at a pipette potential of 60 mV. Lowering pipette Cl- concentration diminished Po to 0.23 ± 0.02 associated with a significant decrease in open time from 0.78 ± 0.03 to 0.61 ± 0.02 s with no significant change in closed time, and shifted the current-voltage relationship leftward. These results suggest that the extracellular Cl- regulates the ENaC-mediated Na+ reabsorption by affecting ENaC properties in AVT-stimulated renal epithelial cells." @default.
• W2053011890 created "2016-06-24" @default.
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• W2053011890 date "2009-01-01" @default.
• W2053011890 modified "2023-09-27" @default.
• W2053011890 title "Effects of extracellular chloride ion on epithelial sodium channel (ENaC) in arginine vasotocin (AVT)-stimulated renal epithelial cells" @default.
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• W2053011890 doi "https://doi.org/10.2220/biomedres.30.193" @default.
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