Evidence for conductive Cl- pathway in the basolateral membrane of rabbit renal proximal tubule S3 segment.
The mechanism of Cl- exit was examined in the basolateral membrane of rabbit renal proximal tubule S3 segment with double-barreled, ion-selective microelectrodes. After the basolateral Cl-/HCO3- exchanger was blocked by 2'-disulfonic acid, a bath K+ step from 5 to 20 mM induced 26.6 mV depolarization and 7.7 mM increase in intracellular Cl- activities ([Cl(-)]i). K+ channel blockers, Ba2+, and quinine strongly suppressed both the response in cell membrane potentials (Vb) and in (Cl-)i to the bath K+ step, while Cl- channel blockers, A9C (1 mM) and IAA-94 (0.3 mM) inhibited only the latter response by 49 and 74%, respectively. By contrast, an inhibitor of K(+)-Cl- cotransporter, H74, had no effect on the increase in (Cl-)i to the bath K+ step. Furosemide and the removal of bath Na+ were also ineffective, suggesting that (Cl-)i are sensitive to the cell potential changes. Bath Cl- removal in the presence of quinine induced a depolarization of more than 10 mV and a decrease in (Cl-)i, and IAA-94 inhibited these responses similarly in the bath K+ step experiments. These results indicate that a significant Cl- conductance exists in the basolateral membrane of this segment and functions as a Cl- exit mechanism.
First Department of Internal Medicine, Tokyo University School of Medicine, Japan.
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Seki
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Taniguchi
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Uwatoko
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Suzuki
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Kurokawa
D000818:Animals; D001464:Barium / Q000494:pharmacology; D016764:Cell Polarity; D002712:Chlorides / Q000378:metabolism*; D004553:Electric Conductivity; D006863:Hydrogen-Ion Concentration; D007687:Kidney Tubules, Proximal / Q000378:metabolism*; D008297:Male; D011188:Potassium / Q000378:metabolism; D011803:Quinine / Q000494:pharmacology; D011817:Rabbits
D002712:Chlorides; D001464:Barium; D011803:Quinine; D011188:Potassium