Acetazolamide and transient responses of basolateral membrane potential of rabbit kidney proximal tubules perfused in vitro.

1. A study was made of the partial recovery of basolateral membrane potential that follows some depolarizing manoeuvres in cells of isolated perfused segments of rabbit proximal convoluted tubules. 2. Peritubular application of 10(-4) M-acetazolamide (a known inhibitor of the basolateral sodium-bicarbonate co-transporter) caused a hyperpolarization of both the basolateral membrane potential (Vbl) and the transepithelial potential (Vte). 3. Activation of electrogenic apical sodium co-transport caused a depolarization of the basolateral membrane followed by partial recovery of potential, and a sustained transepithelial hyperpolarization. The partial recovery of basolateral membrane potential was significantly smaller in the presence of 10(-4) M-acetazolamide applied to the peritubular fluid, although the magnitude of the initial depolarization was not significantly altered. 4. Addition to the bath of 0.5 mM-barium, a potassium conductance blocker, caused a transepithelial and basolateral membrane depolarization followed by partial recovery of potential. The partial recovery of basolateral membrane potential was significantly smaller in the presence of 10(-4) M-acetazolamide applied to the peritubular fluid, although the magnitude of the initial depolarization was again not significantly altered. 5. Increases in bath potassium concentration from 5 to 20 mM led to transepithelial and basolateral membrane depolarization followed by partial recovery of potentials. In paired experiments the partial recovery of basolateral potential was significantly reduced when 10(-4) M-acetazolamide was present in the bath. 6. These observations are consistent with the hypothesis that the basolateral sodium-bicarbonate co-transporter plays a role in the recovery of Vbl following these depolarizing manoeuvres.