Affiliation:
1. Laboratory of Physiology, Katholieke Universiteit Leuven, Campus Gasthuisberg, B-3000 Leuven, Belgium
2. Laboratory of Physiology, Limburgs Universitair Centrum, B-3590 Diepenbeek; and
Abstract
We report, for the epithelial Na+ channel (ENaC) in A6 cells, the modulation by cell pH (pHc) of the transepithelial Na+ current ( I Na), the current through the individual Na+channel ( i), the open Na+ channel density ( N o), and the kinetic parameters of the relationship between I Na and the apical Na+ concentration. The i and N o were evaluated from the Lorentzian I Na noise induced by the apical Na+ 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 Na+/H+exchanger (Na+ removal; block by ethylisopropylamiloride) and were measured with the pH-sensitive probe 2′,7′-bis(2-carboxyethyl)-5(6)-carboxyfluorescein. The changes in pHc were positively correlated to changes in I Na and the apically dominated transepithelial conductance. The sole pHc-sensitive parameter underlying I Na was N o. Only the saturation value of the I Na kinetics was subject to changes in pHc. pHc-dependent changes in N o may be caused by influencing P o, the ENaC open probability, or/and the total channel number, N T = N o/ P o.
Publisher
American Physiological Society
Cited by
16 articles.
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