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      Effects of Changes in Dietary Intake of Sodium and Potassium and of Metabolic Acidosis on 11β-Hydroxysteroid Dehydrogenase Activities in Rat Kidney

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          Abstract

          Background/Aim: Glucocorticoid activity is modulated by NADP<sup>+</sup>- and NAD<sup>+</sup>-dependent isoforms of the enzyme 11β-hydroxysteroid dehydrogenase (11βHSD) which convert glucocorticoids to their inactive metabolites. The NAD<sup>+</sup>-dependent isoform, 11βHSD2, is present in the distal nephron where it confers aldosterone specificity on mineralocorticoid receptors. The objective of this study was to establish whether renal 11βHSD activities are affected by changes in sodium and potassium balance and by metabolic acidosis. Methods: Renal 11βHSD activities were measured ex vivo from rats fed normal and high- and low-potassium diets and a low-sodium diet or given 1.5% NH<sub>4</sub>Cl to drink. Results: Rats maintained on high-potassium and low-sodium diets exhibited 59% (p < 0.01) and 28% (p < 0.05) decreases, respectively, in NAD<sup>+</sup>-dependent renal 11βHSD activity (relative to rats fed control diet) with no changes in NADP<sup>+</sup>-dependent cortisol oxidation. Short-term (3 day) and longer-term (10 day) metabolic acidosis also decreased NAD<sup>+</sup>-dependent 11βHSD activity by 50 and 52%, respectively, without affecting NADP<sup>+</sup>-dependent cortisol oxidation. The low-potassium diet had no detectable effect on renal 11βHSD activities. Conclusion: These results suggest that adaptations to a high-potassium or a low-sodium diet and to metabolic acidosis involve decreases in renal 11βHSD2 activity, enhancing the access of glucocorticoids to renal corticosteroid receptors.

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          Most cited references 4

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          Human hypertension caused by mutations in the kidney isozyme of 11 beta-hydroxysteroid dehydrogenase.

          The syndrome of apparent mineralocorticoid excess (AME) is an inherited form of human hypertension thought to result from a deficiency of 11 beta-hydroxysteroid dehydrogenase (11 beta HSD). This enzyme normally converts cortisol to inactive cortisone and is postulated to thus confer specificity for aldosterone upon the mineralocorticoid receptor. We have analysed the gene encoding the kidney isozyme of 11 beta HSD and found mutations on both alleles in nine of 11 AME patients (eight of nine kindreds). These mutations markedly affect enzymatic activity. They thus permit cortisol to occupy the renal mineralocorticoid receptor and thereby cause sodium retention and hypertension.
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            Cloning and tissue distribution of the human 1 lβ-hydroxysteroid dehydrogenase type 2 enzyme

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              • Article: not found

              Characterization of 11β-hydroxysteroid dehydrogenase of human placenta: Evidence for the existence of two species of 11β-hydroxysteroid dehydrogenase

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                Author and article information

                Journal
                EXN
                Nephron Exp Nephrol
                10.1159/issn.1660-2129
                Cardiorenal Medicine
                S. Karger AG
                1660-2129
                2000
                February 2000
                14 January 2000
                : 8
                : 1
                : 44-51
                Affiliations
                aCentre for Nephrology, The Rayne Institute, Royal Free and University College Medical School, and bDepartment of Biochemistry and Molecular Biology, Royal Free and University College Medical School, London, UK
                Article
                20647 Exp Nephrol 2000;8:44–51
                10.1159/000020647
                10644882
                © 2000 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
                Figures: 5, Tables: 3, References: 29, Pages: 8
                Product
                Self URI (application/pdf): https://www.karger.com/Article/Pdf/20647
                Categories
                Original Paper

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