Abstract
Intracellular microelectrodes were used to investigate rheogenic Na+(HCO 3 ) n cotransport in different segments of isolated proximal straight tubule (PST) of rabbit kidney. In the first portion (S2 segment) the peritubular cell membrane potentialV b averaged −46.0, SE±1.3 mV (n=20), while in the terminal portion (S3 segment) it averaged −68.3, SE±2.5 mV (n=10). This difference may reflect different modes of anion permeation across the peritubular cell membrane. In S2 segments, sudden 10∶1 reduction of bath HCO 3 concentration caused a fast transient cell depolarization, ΔV b=−45.8, SE±1.2 mV (n=33) as expected from the presence of Na+(HCO 3 ) n contransport. As the puncture site moved further distally, ΔV b declined and gradually changed its time course by superposition of a slower secondary depolarization. In this region the transient cell depolarization could be recuperated by inhibiting the peritubular K+ conductance with Ba2+ (1 mmol/l). In S3 segments, however, the HCO 3 -dependent transient cell depolarization was completely lost both in the absence and presence of Ba2+. In addition, sudden reduction of bath Na+ concentration did not acidify the cell, as it did in the S2 segment. The data indicate that the expression of Na+(HCO 3 ) n cotransport in the peritubular cell membrane gradually diminishes towards the end of the S2 segment and is lost in the S3 segment.