This study describes the effects of serosal Cl- and HCO3- substitution on transepithelial Na+ transport and basolateral membrane properties of the rabbit urinary bladder. Replacement of Cl- with NO3-, SCN-, and Br- had no effect on transepithelial Na+ transport or the basolateral membrane potential (Vbl). However, gluconate, isethionate, and cyclamate (anions that were shown previously to be not as permeable as Cl- through the basolateral membrane anion channel), decreased transepithelial Na+ transport and depolarized Vbl. Replacement of HCO3- also produced a decrease in transepithelial Na+ transport and a depolarization of Vbl. Utilizing conventional and K+-specific microelectrodes, we found the depolarization to be due to a reduction in basolateral K+ conductance. This depolarization was reversible only when Cl- was returned to the serosal solution, the normally permeant anion NO3- being unable to affect repolarization, suggesting that both the K+ and Cl- conductance are reduced during depolarization. A lag period of some 4 min preceded the repolarization of Vbl. The Na+-H+ exchange blocker amiloride prolonged the lag phase associated with repolarization, whereas niflumic acid, a Cl-(-)HCO3- exchange blocker (in red blood cells) reduced the magnitude of Vbl repolarization. Because of the possible involvement of the exchangers it is believed that the lag phase represents a volume-dependent and/or pH-dependent reactivation of the basolateral membrane conductances.
