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Research Article Free access | 10.1172/JCI116694

Evidence for conductive Cl- pathway in the basolateral membrane of rabbit renal proximal tubule S3 segment.

G Seki, S Taniguchi, S Uwatoko, K Suzuki, and K Kurokawa

First Department of Internal Medicine, Tokyo University School of Medicine, Japan.

Find articles by Seki, G. in: PubMed | Google Scholar

First Department of Internal Medicine, Tokyo University School of Medicine, Japan.

Find articles by Taniguchi, S. in: PubMed | Google Scholar

First Department of Internal Medicine, Tokyo University School of Medicine, Japan.

Find articles by Uwatoko, S. in: PubMed | Google Scholar

First Department of Internal Medicine, Tokyo University School of Medicine, Japan.

Find articles by Suzuki, K. in: PubMed | Google Scholar

First Department of Internal Medicine, Tokyo University School of Medicine, Japan.

Find articles by Kurokawa, K. in: PubMed | Google Scholar

Published September 1, 1993 - More info

Published in Volume 92, Issue 3 on September 1, 1993
J Clin Invest. 1993;92(3):1229–1235. https://doi.org/10.1172/JCI116694.
© 1993 The American Society for Clinical Investigation
Published September 1, 1993 - Version history
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Abstract

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.

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