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      Increased Expression of Renal Aquaporin Water Channels in Spontaneously Hypertensive Rats

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          Abstract

          Aims: The present study was aimed to determine whether there exists an altered regulation of aquaporin (AQP) water channels in hypertension. Methods: Male spontaneously hypertensive rats (SHR) aged 10–12 weeks were used. Age-matched Wistar-Kyoto (WKY) rats served as control. The abundance of AQP1–4 proteins in the kidney was determined by Western blot analysis. The protein expression and activity of adenylyl cyclase were also determined. Results: The medullary expression of AQP2 and AQP3 proteins was increased in SHR compared with that in WKY rats. The expression of AQP1 protein was also significantly increased in the inner medulla, while that of AQP4 was not. Immunohistochemistry of AQP2 revealed that principal cells of the collecting duct have strong immunoreactivity, the degree of which was augmented with prominent apical labeling in SHR. The plasma level of arginine vasopressin (AVP) was higher in SHR; the adenylyl cyclase activity stimulated by AVP was augmented, along with increased expression of type VI adenylyl cyclase. The urine was more concentrated with its volume decreased in SHR. Conclusion: The expression of AQP1–3 channels is increased in the kidney, in association with enhanced activity of the AVP/cAMP pathway, in SHR.

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          Cloned and expressed nitric oxide synthase structurally resembles cytochrome P-450 reductase.

          C L Lowenstein, Charles Glatt, Jessica Hwang … (1991)
          Nitric oxide is a messenger molecule, mediating the effect of endothelium-derived relaxing factor in blood vessels and the cytotoxic actions of macrophages, and playing a part in neuronal communication in the brain. Cloning of a complementary DNA for brain nitric oxide synthase reveals recognition sites for NADPH, FAD, flavin mononucleotide and calmodulin as well as phosphorylation sites, indicating that the synthase is regulated by many different factors. The only known mammalian enzyme with close homology is cytochrome P-450 reductase.
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            Cellular and subcellular immunolocalization of vasopressin-regulated water channel in rat kidney.

            M A Knepper, S. Nielsen, E Christensen … (1993)
            Article 0 comments Cited 55 times – based on 0 reviews     Review now
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              Long term regulation of aquaporin-2 expression in vasopressin-responsive renal collecting duct principal cells.

              Jean-Pierre Martin, Eric Féraille, Françoise Cluzeaud … (2002)
              Fine regulation of water reabsorption by the antidiuretic hormone [8-arginine]vasopressin (AVP) occurs in principal cells of the collecting duct and is largely dependent on regulation of the aquaporin-2 (AQP2) water channel. AVP-inducible long term AQP2 expression was investigated in immortalized mouse cortical collecting duct principal cells. Combined RNase protection assay, Western blot, and immunofluorescence analyses revealed that physiological concentrations of AVP added to the basal side, but not to the apical side, of cells grown on filters induced both AQP2 mRNA and apical protein expression. The stimulatory effect of AVP on AQP2 expression followed a V(2) receptor-dependent pathway because [deamino-8-d-arginine]vasopressin (dDAVP), a specific V(2) receptor agonist, produced the same effect as AVP, whereas the V(2) antagonist SR121463B antagonized action of both AVP and dDAVP. Moreover, forskolin and cyclic 8-bromo-AMP fully reproduced the effects of AVP on AQP2 expression. Analysis of protein degradation pathways showed that inhibition of proteasomal activity prevented synthesis of AVP-inducible AQP2 mRNA and protein. Once synthesized, AQP2 protein was quickly degraded, a process that involves both the proteasomal and lysosomal pathways. This is the first study that delineates induction and degradation mechanisms of AQP2 endogenously expressed by a renal collecting duct principal cell line.
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                Author and article information

                Journal
                Journal ID (publisher-id): KBR
                Journal ID (nlm-ta): Kidney Blood Press Res
                Journal ID (doi): 10.1159/issn.1420-4096
                Title: Kidney and Blood Pressure Research
                Publisher: S. Karger AG
                ISSN (Print): 1420-4096
                ISSN (Electronic): 1423-0143
                Publication date Subscription-year: 2006
                Publication date (Print): June 2006
                Publication date (Electronic): 06 June 2006
                Volume: 29
                Issue: 1
                Pages: 18-23
                Affiliations
                Departments of aPhysiology and cInternal Medicine, Chonnam National University Medical School, Gwangju, and bDepartment of Anatomy, Catholic Medical University, Seoul, Korea
                Article
                Publisher ID: 92483 Other ID: Kidney Blood Press Res 2006;29:18–23
                DOI: 10.1159/000092483
                PubMed ID: 16582573
                SO-VID: 8f1f1cf8-8a80-4c90-a8c2-4031177abf9f
                Copyright © © 2006 S. Karger AG, Basel
                License:

                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.

                History
                Date received : 03 August 2005
                Date accepted : 22 December 2005
                Page count
                Figures: 3, Tables: 2, References: 25, Pages: 6
                Categories
                Subject: Original Paper

                ScienceOpen disciplines: Cardiovascular Medicine,Nephrology
                Keywords: Spontaneously hypertensive rat,Aquaporin water channels,Adenylyl cyclase
                Data availability:
                ScienceOpen disciplines: Cardiovascular Medicine, Nephrology
                Keywords: Spontaneously hypertensive rat, Aquaporin water channels, Adenylyl cyclase

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