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Abstract

Intracellular microelectrodes were used to investigate rheogenic Na⁺ (HCO₃^-)_n cotransport in different segments of isolated proximal straight tubule (PST) of rabbit kidney. In the first portion (S2 segment) the peritubular cell membrane potential V_b averaged -46.0, SE ± 1.3 mV (n = 20), while in 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 HCO₃^- concentration caused a fast transient cell depolarization, delta V_b = -45.8, SE ± 1.2 mV (n = 33) as expected from the presence of Na⁺ (HCO₃^-)_n cotransport. As the puncture site moved further distally, delta V_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 HCO₃^--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⁺ (HCO₃^-)_n cotransport in the peritubular cell membrane gradually diminishes towards the end of the S2 segment and is lost in the S3 segment.