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      Glutamate Metabolism and Ammonia Production in Dog Kidneys

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      Nephron

      S. Karger AG

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          Abstract

          In vivo, over a short 2-hour period, renal ammonia production in dogs increased (+41%) and renal glutamate concentrations decreased (-21%) following acid challenge. Since glutamate is an inhibitor of glutamine deamidating enzyme, glutaminase I, these results are compatible with the concept that during acid challenge, lowered concentrations of glutamate increase ammoniagenesis via accelerated glutamine deamidation. However, glutamate infusions in vivo into dogs do not alter ammoniagenesis from glutamine. To explain this paradox, evidence is presented that exogenous glutamate does not reach ammonia producing sites. In vivo, exogenous glutamate neither increases nor decreases renal ammonia production; whereas exogenous alanine, which must form glutamate through transamination in order to be deaminated, produces a good deal of ammonia. That both the amino nitrogen of glutamine and the amino nitrogen of alanine produced more ammonia than the amino nitrogen of glutamate at equimolar concentrations in isolated dog tubules suggests that there is a relative impermeability of glutamate to ammonia producing sites even in vitro. Despite this relative barrier, dog tubules do produce ammonia from glutamate allowing one to conclude that this substrate does reach ammonia producing sites in vitro. Here, exogenous glutamate added to incubation medium did depress utilization of glutamine significantly. We conclude that there may be an important role for glutamate concentrations at ammonia producing sites in regulating renal ammoniagenesis.

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          Author and article information

          Journal
          NEF
          Nephron
          10.1159/issn.1660-8151
          Nephron
          S. Karger AG
          1660-8151
          2235-3186
          1971
          1971
          26 November 2008
          : 8
          : 4
          : 344-354
          Affiliations
          Renal Metabolism Laboratory, Renal and Electrolyte Division, Department of Medicine of the University of Pittsburgh School of Medicine, Pittsburgh, Pa.
          Article
          179937 Nephron 1971;8:344–354
          10.1159/000179937
          5094850
          © 1971 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: 11
          Categories
          Paper

          Cardiovascular Medicine, Nephrology

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