Antracene-9-carboxylic acid inhibits renal chloride reabsorption

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Abstract
From previous studies, it is known that in the diluting segment, Cl−-ions are transported from the tubule lumen into the cell together with Na+ and K+ via a furosemide-sensitive cotransport system. This carrier-mediated process, located in the luminal cell membrane, is driven by the steep “downhill” Na+ gradient (directed from lumen to cell) which is maintained by the ouabain-sensitive Na+/K+-pump at the peritubular cell membrane. Cl−-ions are accumulated within the cell cytosol and are supposed to leave the cell by a Cl−-conductive pathway. The present experiments, performed in diluting segments of the isolated perfused frog kidney, demonstrate the existence of a significant Cl−-permeability of the peritubular cell membrane and its complete inhibition by anthracene-9-COOH. The data indicate that Cl−-reabsorption can be reduced not only by the inhibition of luminal Cl−-entry (i.e. by furosemide) but also by the blockade of the passive Cl−-exit step across the peritubular cell membrane. Since complete inhibition of Cl−-permeability reduces transepithelial uphill Cl−-transport only to half, the data disclose the existance of an additional Cl−-pathway at the peritubular cell membrane.

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