Anthracene-9-carboxylic acid inhibits renal chloride reabsorption.
From previous studies, it is known that in the diluting segment, C1- -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. C1- -ions are accumulated within the cell cytosol and are supposed to leave the cell by a C1- -conductive pathway. The present experiments, performed in diluting segments of the isolated perfused frog kidney, demonstrate the existence of a significant C1- -permeability of the peritubular cell membrane and its complete inhibition by anthracene-9-COOH. The data indicate that C1- -reabsorption can be reduced not only by the inhibition of luminal C1- -entry (i.e. by furosemide) but also by the blockade of the passive C1- -exit step across the peritubular cell membrane. Since complete inhibition of C1- -permeability reduces transepithelial uphill C1- -transport only to half, the data disclose the existence of an additional C1- -pathway at the peritubular cell membrane.
D000818:Animals; D000873:Anthracenes / Q000494:pharmacology*; D002463:Cell Membrane Permeability / Q000187:drug effects*; D002712:Chlorides / Q000378:metabolism*; D066298:In Vitro Techniques; D007668:Kidney / Q000166:cytology / Q000378:metabolism*; D011893:Rana esculenta
D000873:Anthracenes; D002712:Chlorides; C010030:9-anthroic acid