Mechanisms of voltage transients during current clamp in Necturus gallbladder.

Microelectrode techniques were employed to study the mechanisms of the transepithelial voltage transients (deltaVms) observed during transmural current clamps in the isolated Necturus gallbladder. The results indicate that: a) part of deltaVms is due to a transepithelial resistance change (deltaRt), and part to a tissue emf change. b) deltaRt is entirely caused by changes of the resistance of the paracellular pathway. At all current densities employed, the measured changes are probably due to changes in both fluid conductivity and width of the lateral intercellular spaces. At high currents, in addition to the effects on the lateral spaces, the resistance of other elements of the pathway (probably the limiting junction) drops, regardless of the direction of the current. c) The magnitude and polarity of the deltaRt-independent transepithelial and cell membrane potential transients indicate that the largest emf change takes place at the basolateral membrane (deltaEb), with smaller changes at the luminal membrane (deltaEa) and the paracellular (shunt) pathway (deltaEs). It is shown that two-thirds of the transient are caused by deltaEs, and one-third by delta(Eb--Ea). deltaEs can be explained by a diffusion potential generated by a current-dependent NaCl concentration gradient across the tissue. deltaEa and deltaEb are caused by [K] changes, mainly at the unstirred layer in contact with the basolateral membrane.