The effects of chloride ions on electrodiffusion in the membrane of a leaky epithelium. Studies of intact tissue by microelectrodes.

The electrodiffusive permeability 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 of Necturus 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 X 10(-6) cm s-1. This permeability together with the K+-permeability of the ventricular membrane (24 X 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-3 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 Clv was a tenfold increase of the electrodiffusive Cl--permeability of the ventricular membrane to 12.2 X 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 HCO-3/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+.