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      Regulation of Proximal Renal Tubular K + Conductance by Intracellular pH

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          Abstract

          Conventional electrophysiology and 2’, 7’-bis-(2-carboxyethyl)-5-(and 6)-carboxyfluorescein fluorescence have been applied to elucidate the effects of metabolic acidosis on straight proximal tubules of the mouse kidney. Reduction of extracellular bicarbonate concentration from 20 to 10 mmol/l leads to a decline of intracellular pH from 7.00+0.06 to 6.85 ± 0.05, a depolarization of the cell membrane (PDb1) from –72 ± 1 to -59 ± 2 mV, a decrease of the basolateral transference number for potassium (tK) from 0.80 ± 0.01 to 0.54 ± 0.03, an increase of the basolateral transference number for bicarbonate (tb) from 0.16 ± 0.02 to 0.42 ± 0.03 and an increase of the fractional resistance of the basolateral over the luminal cell membrane (Rb/Ra) by 64 ± 8%. Upon return to 20 mmol/l bicarbonate after a 5-min exposure to 10 mmol/l bicarbonate, the intracellular pH approached a more alkaline value (7.28 ± 0.08) than before exposure to acidosis. Despite the intracellular alkalosis, PDb1 (-67 ± 1 mV) and tK (0.73 ± 0.02) remained significantly below, and tb (0.26 ± 0.02) and Rb/Ra (32 ± 8%) significantly above the respective values before induction of acidosis. Even transient exposure of the tubules to 40 mmol/l extracellular bicarbonate did not restore the original electrophysiological properties of the tubule cells. It is concluded that both a rapidly reversible and a long-lasting decrease of proximal tubular K<sup>+</sup> conductance follows cellular acidosis.

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          Author and article information

          Journal
          NEF
          Nephron
          10.1159/issn.1660-8151
          Nephron
          S. Karger AG
          1660-8151
          2235-3186
          1994
          1994
          17 December 2008
          : 68
          : 2
          : 234-238
          Affiliations
          aInstitut für Physiologie der Universität Innsbruck, Österreich; bPhysiologisches Institut der Universität Tübingen, Deutschland
          Article
          188263 Nephron 1994;68:234–238
          10.1159/000188263
          7830862
          © 1994 S. Karger AG, Basel

          Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

          Page count
          Pages: 5
          Categories
          Original Paper

          Cardiovascular Medicine, Nephrology

          Cell membrane potential, Bicarbonate selectivity, Acidosis

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