Intracellular sodium activity and sodium transport in necturus gallbladder epithelium.

Abstract

Ion-sensitive glass microelectrodes, conventional microelectrodes and isotope flux measurements were employed inNecturus gallbladder epithelium to study intracellular sodium activity, [Na]i, electrical parameters of epithelial cells, and properties of active sodium transport. Mean control values were: [Na]i: 9.2 to 12.1mm; transepithelial potential difference,Ψms: −1.5 mV (lumen negative); basolateral cell membrane potential,Ψes: −62 mV (cell interior negative); sodium conductance of the luminal cell membrane,gNa: 12 μmho cm−2; active transcellular sodium flux, 88 to 101 pmol cm−2 sec−1 (estimated as instantaneous short-circuit current). Replacement of luminal Na by K led to a decrease of the intracellular sodium activity at a rate commensurate to the rate of active sodium extrusion across the basolateral cell membrane. Mucosal application of amphotericin B resulted in an increase of the luminal membrane conductance, a rise of intracellular sodium activity, and an increase of short-circuit current and unidirectional mucosa to serosa sodium flux. Conclusions: (i) sodium transport across the basolateral membrane can proceed against a steeper chemical potential difference at a higher rate than encountered under control conditions; (ii) the luminal Na-conductance is too low to accommodate sodium influx at the rate of active basolateral sodium extrusion, suggesting involvement of an electrically silent luminal transport mechanism; (iii) sodium entry across the luminal membrane is the rate-limiting step of transcellular sodium transport and active sodium extrusion across the basolateral cell membrane is not saturated under control conditions.