ACELL September 46/3

نویسندگان

  • WOLFGANG ZEISKE
  • ILSE SMETS
  • MARCEL AMELOOT
  • PAUL STEELS
  • WILLY VAN DRIESSCHE
  • Ilse Smets
  • Marcel Ameloot
چکیده

Zeiske, Wolfgang, Ilse Smets, Marcel Ameloot, Paul Steels, and Willy Van Driessche. Intracellular pH shifts in cultured kidney (A6) cells: effects on apical Na1 transport. Am. J. Physiol. 277 (Cell Physiol. 46): C469–C479, 1999.—We report, for the epithelial Na1 channel (ENaC) in A6 cells, the modulation by cell pH (pHc) of the transepithelial Na1 current (INa), the current through the individual Na1 channel (i), the open Na1 channel density (No), and the kinetic parameters of the relationship between INa and the apical Na1 concentration. The i and No were evaluated from the Lorentzian INa noise induced by the apical Na1 channel blocker 6-chloro-3,5-diaminopyrazine-2-carboxamide. pHc shifts were induced, under strict and volume-controlled experimental conditions, by apical/basolateral NH4Cl pulses or basolateral arrest of the Na1/H1 exchanger (Na1 removal; block by ethylisopropylamiloride) and were measured with the pH-sensitive probe 28,78-bis(2-carboxyethyl)-5(6)-carboxyfluorescein. The changes in pHc were positively correlated to changes in INa and the apically dominated transepithelial conductance. The sole pHc-sensitive parameter underlying INa was No. Only the saturation value of the INa kinetics was subject to changes in pHc. pHc-dependent changes in No may be caused by influencing Po, the ENaC open probability, or/and the total channel number, NT 5 No/Po.

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تاریخ انتشار 1999