The effects of chloride ions on electrodiffusion in the membrane of a leaky epithelium

Abstract

The electrodiffusive permeabiilty for Cl⁻, its dependence on low extracellular Cl⁻-concentrations and the interaction between the movements of Cl⁻ and K⁺ were investigated in the ventricular membrane of epithelial cells from the choroid plexus ofNecturus maculosus. Cells were probed with ion-selective microelectrodes sensitive to Cl⁻, K⁺ and H⁺. The initial effects of abrupt changes in the Cl⁻-concentration (Cl ⁻_v ) and/or the K⁺-concentration (K ⁺_v ) of the ventricular solution were investigated. The effect of changing the membrane potential by changing K ⁺_v was twofold: It caused an electrodiffusive flux of Cl⁻ via a permeability of 1.3 × 10⁻⁶ cm s⁻¹. This permeability together with the K⁺-permeability of the ventricular membrane (24 × 10⁻⁶ cm s⁻¹) determined the membrane potential in the given steady state within a few mV. The other effect of the depolarization was an increase in the intracellular concentration of HCO ⁻¹₃ which in turn caused an influx of Cl⁻ via electroneutral Cl⁻/HCO ⁻₃ exchange. The Cl⁻-permeability was reduced by more than 60% and the neutral exchange by more than 90% by furosemide. The effect of decreases in Cl_v was a tenfold increase of the electrodiffusive Cl⁻-permeability of the ventricular membrane to 12.2 × 10⁻⁶ cm s⁻¹ and also a tenfold increase in the permeability to K⁺. This activation was reduced by two thirds by furosemide, and by depolarizations of the cell by high K_v ⁺. In the given steady state the HCO₃ ⁻/Cl⁻ exchanger at the ventricular membrane transports at a rate of 300 pmol cm⁻² s⁻¹ and moves Cl⁻ into the cell and HCO ⁻₃ into the ventricular solution. Thus the epithelium alkalinizes the cerebrospinal fluid at a rate which is about three times faster than the net transport rate of Na⁺.