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      Call for Papers: Green Renal Replacement Therapy: Caring for the Environment

      Submit here before July 31, 2024

      About Blood Purification: 3.0 Impact Factor I 5.6 CiteScore I 0.83 Scimago Journal & Country Rank (SJR)

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      Effects of Combined Endothelin A Receptor and Renin-Angiotensin System Blockade on the Course of End-Organ Damage in 5/6 Nephrectomized Ren-2 Hypertensive Rats

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          Abstract

          Our previous studies in rats with ablation nephrectomy have shown similar cardiorenal protective effects of renin-angiotensin system (RAS)-dependent treatment (combination of angiotensin-converting enzyme inhibitor and angiotensin II receptor blocker) and RAS-independent treatment (combination of α- and β-adrenoreceptor antagonist and diuretics). Moreover, selective blockade of endothelin (ET) receptor type A (ET<sub>A</sub>) improved survival rate and attenuated hypertension and organ damage in Ren-2 transgenic rats. Therefore, we were interested in whether ET<sub>A</sub> receptor blockade could have additive effects to the classical blockade of the RAS. Transgenic rats underwent 5/6 renal ablation at the age of 2 months and were treated for 20 weeks with RAS blockers alone (angiotensin II receptor blocker – losartan, and angiotensin-converting enzyme inhibitor – trandolapril), ET<sub>A</sub> receptor blocker alone (atrasentan) or with the combination of RAS and ET<sub>A</sub> receptor blockade. RAS blockade normalized blood pressure and improved survival. It decreased cardiac hypertrophy and proteinuria as well as tissue angiotensin II and ET-1 levels. In contrast, ET<sub>A</sub> receptor blockade only partially improved survival rate, reduced blood pressure, attenuated the development of cardiac hypertrophy and transiently reduced proteinuria. However, no additive cardio- and renoprotective effects of ET<sub>A</sub> and RAS blockade were noted at the end of the study.

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          The intrarenal renin-angiotensin system: from physiology to the pathobiology of hypertension and kidney disease.

          Hiroyuki Kobori, Masaomi Nangaku, L. Gabriel Navar … (2007)
          In recent years, the focus of interest on the role of the renin-angiotensin system (RAS) in the pathophysiology of hypertension and organ injury has changed to a major emphasis on the role of the local RAS in specific tissues. In the kidney, all of the RAS components are present and intrarenal angiotensin II (Ang II) is formed by independent multiple mechanisms. Proximal tubular angiotensinogen, collecting duct renin, and tubular angiotensin II type 1 (AT1) receptors are positively augmented by intrarenal Ang II. In addition to the classic RAS pathways, prorenin receptors and chymase are also involved in local Ang II formation in the kidney. Moreover, circulating Ang II is actively internalized into proximal tubular cells by AT1 receptor-dependent mechanisms. Consequently, Ang II is compartmentalized in the renal interstitial fluid and the proximal tubular compartments with much higher concentrations than those existing in the circulation. Recent evidence has also revealed that inappropriate activation of the intrarenal RAS is an important contributor to the pathogenesis of hypertension and renal injury. Thus, it is necessary to understand the mechanisms responsible for independent regulation of the intrarenal RAS. In this review, we will briefly summarize our current understanding of independent regulation of the intrarenal RAS and discuss how inappropriate activation of this system contributes to the development and maintenance of hypertension and renal injury. We will also discuss the impact of antihypertensive agents in preventing the progressive increases in the intrarenal RAS during the development of hypertension and renal injury.
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            Mechanisms of progression and regression of renal lesions of chronic nephropathies and diabetes.

            Giuseppe Remuzzi, Ariela Benigni, Andrea Remuzzi (2006)
            The incidence of chronic kidney diseases is increasing worldwide, and these conditions are emerging as a major public health problem. While genetic factors contribute to susceptibility and progression of renal disease, proteinuria has been claimed as an independent predictor of outcome. Reduction of urinary protein levels by various medications and a low-protein diet limits renal function decline in individuals with nondiabetic and diabetic nephropathies to the point that remission of the disease and regression of renal lesions have been observed in experimental animals and even in humans. In animal models, regression of glomerular structural changes is associated with remodeling of the glomerular architecture. Instrumental to this discovery were 3D reconstruction studies of the glomerular capillary tuft, which allowed the quantification of sclerosis volume reduction and capillary regeneration upon treatment. Regeneration of capillary segments might result from the contribution of resident cells, but progenitor cells of renal or extrarenal origin may also have a role. This review describes recent advances in our understanding of the mechanisms and mediators underlying renal tissue repair ultimately responsible for regression of renal injury.
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              Regulation of blood pressure and salt homeostasis by endothelin.

              Donald Kohan, Marcelo Rossi, Edward W. Inscho … (2010)
              Endothelin (ET) peptides and their receptors are intimately involved in the physiological control of systemic blood pressure and body Na homeostasis, exerting these effects through alterations in a host of circulating and local factors. Hormonal systems affected by ET include natriuretic peptides, aldosterone, catecholamines, and angiotensin. ET also directly regulates cardiac output, central and peripheral nervous system activity, renal Na and water excretion, systemic vascular resistance, and venous capacitance. ET regulation of these systems is often complex, sometimes involving opposing actions depending on which receptor isoform is activated, which cells are affected, and what other prevailing factors exist. A detailed understanding of this system is important; disordered regulation of the ET system is strongly associated with hypertension and dysregulated extracellular fluid volume homeostasis. In addition, ET receptor antagonists are being increasingly used for the treatment of a variety of diseases; while demonstrating benefit, these agents also have adverse effects on fluid retention that may substantially limit their clinical utility. This review provides a detailed analysis of how the ET system is involved in the control of blood pressure and Na homeostasis, focusing primarily on physiological regulation with some discussion of the role of the ET system in hypertension.
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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: 2012
                Publication date (Print): June 2012
                Publication date (Electronic): 04 April 2012
                Volume: 35
                Issue: 5
                Pages: 382-392
                Affiliations
                aInstitute of Physiology v.v.i., Academy of Sciences of the Czech Republic, bCardiovascular Research Center, cDepartment of Pathology, 3rd Faculty of Medicine, dDepartment of Nephrology, 1st Faculty of Medicine, eDepartment of Physiology, 2nd Medical Faculty, Charles University, and fDepartment for Experimental Medicine, Institute for Clinical and Experimental Medicine, Prague, Czech Republic; gSection of Nephrology, Medical Policlinic, Department of Medicine, University of Bonn, Bonn, Germany
                Author notes
                *Ivana Vaneckova, PhD, Institute of Physiology v.v.i., Academy of Sciences of the Czech Republic, Videnska 1083, CZ–14220 Prague 4 (Czech Republic), Tel. +420 24 106 2666, E-Mail ivanava@biomed.cas.cz
                Article
                Publisher ID: 336823 Other ID: Kidney Blood Press Res 2012;35:382–392
                DOI: 10.1159/000336823
                PubMed ID: 22487948
                SO-VID: 19d6b9ee-3d2a-4bed-8a68-d6f1a0584c9c
                Copyright © © 2012 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 : 04 November 2011
                Date accepted : 26 January 2012
                Page count
                Figures: 4, Pages: 11
                Categories
                Subject: Original Paper

                ScienceOpen disciplines: Cardiovascular Medicine,Nephrology
                Keywords: 5/6 nephrectomy,End-organ damage,Hypertension,Endothelin receptor type A,AT1 receptor blocker
                Data availability:
                ScienceOpen disciplines: Cardiovascular Medicine, Nephrology
                Keywords: 5/6 nephrectomy, End-organ damage, Hypertension, Endothelin receptor type A, AT1 receptor blocker

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