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Renal proximal tubule S3 segment; Cell; pH; Intracellular Cl− activity; Basolateral cell membrane; Cl−/HCO−3 exchange
Abstract:
The mechanism of HCO−3 exit from rabbit renal proximal tubule S3 segments was investigated. Isolated tubules were perfused luminally and peritubularly with test solutions and cell pH (pHi), cell Cl− activity ([Cl−]i) and cell Na+ activity ([Na+]i) were measured with ion-selective microelectrodes. From the response of pHi and [Cl−]i to changes in bath Cl− or HCO−3 concentrations a Cl−/HCO−3 exchanger was identified in the basolateral cell membrane. It was reversibly inhibited by millimolar concentrations of the disulfonic stilbene SITS (4-acetamido-4′-isothiocyanato-stilbene-2,2′-disulfonic acid). Cell potential measurements and preliminary determinations of initial ion flux rates suggested a stoichiometry of Cl− to HCO−3 flux near 1.0. The transport rate appeared to saturate already at low bath Cl− concentrations (≈30 mmol/l), but it was independent of bath pH in the range of 7.4-6.4. Cl−/HCO−3 exchange was not directly coupled to Na+ flux although in approximately half of the experiments long-term incubation in Na+-free solutions indirectly inhibited the exchanger. Sudden application of SITS under control conditions revealed that the exchanger normally facilitates the exit of HCO−3 from cell to interstitium at the expense of Cl− uptake into the cell. How Cl− ions recirculate towards the peritubular surface is presently not known.
