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      Oxidative Stress Status in Kidney Tissue after Losartan and Atenolol Treatment in Experimental Renal Failure

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          Abstract

          Background/Aims: Rats with subtotal nephrectomy (5/6NPX) rapidly develop systemic hypertension and proteinuria. The aim of our study was to evaluate the changes in oxidative stress parameters after 2 and 4 weeks of treatment with renin-angiotensin system (RAS)-blocking agent losartan and beta-blocking agent atenolol in experimental chronic renal failure (CRF). Methods: After 5/6NPX, rats were immediately treated with losartan or atenolol. The lipid peroxidation (LPO) products malondialdehyde and 4-hydroxyalkenals and oxidized and reduced glutathione values were measured in the renal cortex tissue and in blood; isoprostanes in urine. Results: There were no differences in the blood pressure values, serum creatinine levels or in daily proteinuria using both antihypertensive treatments. Losartan treatment lowered significantly LPO in kidney tissue after 2 and 4 weeks of treatment compared with untreated and atenolol-treated animals and induced the decrease of excretion of isoprostanes in urine at the end of the study. There was no ameliorating impact of losartan or atenolol observed in the blood status of oxidative stress in this period of time. Conclusion: In the early period of experimental CRF, losartan treatment but not atenolol treatment induces significant decline in LPO grade in the kidney tissue of nephrectomized rats. RAS blockade in the kidney influences local tissue LPO in a much greater extent than in blood.

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          Most cited references 5

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          The elephant in uremia: oxidant stress as a unifying concept of cardiovascular disease in uremia.

          Cardiovascular disease is the leading cause of mortality in uremic patients. In large cross-sectional studies of dialysis patients, traditional cardiovascular risk factors such as hypertension and hypercholesterolemia have been found to have low predictive power, while markers of inflammation and malnutrition are highly correlated with cardiovascular mortality. However, the pathophysiology of the disease process that links uremia, inflammation, and malnutrition with increased cardiovascular complications is not well understood. We hereby propose the hypothesis that increased oxidative stress and its sequalae is a major contributor to increased atherosclerosis and cardiovascular morbidity and mortality found in uremia. This hypothesis is based on studies that conclusively demonstrate an increased oxidative burden in uremic patients, before and particularly after renal replacement therapies, as evidenced by higher concentrations of multiple biomarkers of oxidative stress. This hypothesis also provides a framework to explain the link that activated phagocytes provide between oxidative stress and inflammation (from infectious and non-infections causes) and the synergistic role that malnutrition (as reflected by low concentrations of albumin and/or antioxidants) contributes to the increased burden of cardiovascular disease in uremia. We further propose that retained uremic solutes such as beta-2 microglobulin, advanced glycosylated end products (AGE), cysteine, and homocysteine, which are substrates for oxidative injury, further contribute to the pro-atherogenic milieu of uremia. Dialytic therapy, which acts to reduce the concentration of oxidized substrates, improves the redox balance. However, processes related to dialytic therapy, such as the prolonged use of catheters for vascular access and the use of bioincompatible dialysis membranes, can contribute to a pro-inflammatory and pro-oxidative state and thus to a pro-atherogenic state. Anti-oxidative therapeutic strategies for patients with uremia are in their very early stages; nonetheless, early studies demonstrate the potential for significant efficacy in reducing cardiovascular complications.
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            Renal oxygenation defects in the spontaneously hypertensive rat: role of AT1 receptors.

            The spontaneously hypertensive rat (SHR) has oxidative stress and enhanced O2 usage (Q(O2)) relative to tubular sodium transport (TNa). Angiotensin II (Ang II) acting on Type I receptors (AT1-R) causes renal oxidative stress and functional nitric oxide (NO) deficiency that could enhance O2 usage. Therefore, we investigated the hypothesis that AT1-Rs mediate the inefficient renal oxygenation in the SHR.
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              • Article: not found

              Oxidative stress in juvenile essential hypertension

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                Author and article information

                Journal
                NEE
                Nephron Exp Nephrol
                10.1159/issn.1660-2129
                Cardiorenal Medicine
                S. Karger AG
                1660-2129
                2004
                June 2004
                17 November 2004
                : 97
                : 2
                : e33-e37
                Affiliations
                aDepartment of Sports Medicine and Rehabilitation, bInstitute of Anatomy and Histology, cInstitute of Pathology, dBiochemistry Institute and eDepartment of Internal Medicine, University of Tartu, Tartu, Estonia
                Article
                78404 Nephron Exp Nephrol 2004;97:e33–e37
                10.1159/000078404
                15218321
                © 2004 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
                Tables: 3, References: 17, Pages: 1
                Product
                Self URI (application/pdf): https://www.karger.com/Article/Pdf/78404
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