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      Knockout of Angiotensin 1–7 Receptor Mas Worsens the Course of Two-Kidney, One-Clip Goldblatt Hypertension: Roles of Nitric Oxide Deficiency and Enhanced Vascular Responsiveness to Angiotensin II

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          Abstract

          Aims: The present study was performed to evaluate the effects of target disruption of the G-protein-coupled receptor Mas for angiotensin 1–7 [Ang(1–7)] in knockout mice on the course of two-kidney, one-clip (2K1C) Goldblatt hypertension. Methods: Knockout and wild-type mice underwent clipping of one renal artery. Blood pressure (BP) was monitored by radiotelemetry. The mice were either untreated or chronically treated with the superoxide (O<sub>2</sub><sup>–</sup>) scavenger tempol (400 mg/l) or the inhibitor of NADPH oxidase apocynin (1 g/l) administered in drinking water. Results: Knockout mice responded to clipping by accelerated increases in BP and the final BP was significantly higher than that in wild-type mice. Chronic treatment with tempol or apocynin elicited similar antihypertensive effects in 2K1C/knockout as in 2K1C/wild-type mice. Acute nitric oxide synthase inhibition caused greater BP increases in 2K1C/wild-type than in 2K1C/knockout mice. Conclusion: Our present findings support the notion that the angiotensin-converting enzyme 2-Ang(1–7)-Mas axis serves as an important endogenous physiological counterbalancing mechanism that partially attenuates the hypertensinogenic actions of the activated renin-angiotensin system. The impairment in this axis may contribute to the deterioration of the course of 2K1C Goldblatt hypertension.

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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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            Altered blood pressure responses and normal cardiac phenotype in ACE2-null mice.

            L Acton, Nisha Philip, Thomas M. Coffman … (2006)
            The carboxypeptidase ACE2 is a homologue of angiotensin-converting enzyme (ACE). To clarify the physiological roles of ACE2, we generated mice with targeted disruption of the Ace2 gene. ACE2-deficient mice were viable, fertile, and lacked any gross structural abnormalities. We found normal cardiac dimensions and function in ACE2-deficient animals with mixed or inbred genetic backgrounds. On the C57BL/6 background, ACE2 deficiency was associated with a modest increase in blood pressure, whereas the absence of ACE2 had no effect on baseline blood pressures in 129/SvEv mice. After acute Ang II infusion, plasma concentrations of Ang II increased almost 3-fold higher in ACE2-deficient mice than in controls. In a model of Ang II-dependent hypertension, blood pressures were substantially higher in the ACE2-deficient mice than in WT. Severe hypertension in ACE2-deficient mice was associated with exaggerated accumulation of Ang II in the kidney, as determined by MALDI-TOF mass spectrometry. Although the absence of functional ACE2 causes enhanced susceptibility to Ang II-induced hypertension, we found no evidence for a role of ACE2 in the regulation of cardiac structure or function. Our data suggest that ACE2 is a functional component of the renin-angiotensin system, metabolizing Ang II and thereby contributing to regulation of blood pressure.
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              Genetically altered animal models for Mas and angiotensin-(1-7).

              Natalia Alenina, Lan-Ping Xu, Brit Rentzsch … (2008)
              Mas is the receptor for angiotensin-(1-7) and is involved in cardiovascular and neuronal regulation, in which the heptapeptide also plays a major role. Mas-deficient mice have been generated by us, and their characterization has shown that Mas has important functions in behaviour and cardiovascular regulation. These mice exhibit increased anxiety but, despite an enhanced long-term potentiation in the hippocampus, do not perform better in learning experiments. When Mas-deficient mice are backcrossed to the FVB/N genetic background, a cardiovascular phenotype is uncovered, in that the backcrossed animals become hypertensive. Concordant with our detection by fluorescent in situ hybridization of Mas mRNA in mouse endothelium, this phenotype is caused by endothelial dysfunction based on a dysbalance between nitric oxide and reactive oxygen species in the vessel wall. In agreement with these data, transgenic spontaneously hypertensive stroke-prone rats overexpressing ACE2 in the vessel wall exhibit reduced blood pressure as a result of improved endothelial function. Moreover, angiotensin-(1-7) overexpression in transgenic rats has cardioprotective and haemodynamic effects. In conclusion, the angiotensin-(1-7)-Mas axis has important functional implications for vascular regulation and blood pressure control, particularly in pathophysiological situations.
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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: 2010
                Publication date (Print): December 2010
                Publication date (Electronic): 10 November 2010
                Volume: 33
                Issue: 6
                Pages: 476-488
                Affiliations
                a1st Department of Medicine, Thomayer Teaching Hospital, bDepartment for Experimental Medicine, Institute for Clinical and Experimental Medicine, cDepartment of Nephrology, Transplant Center, Institute for Clinical and Experimental Medicine, dCenter for Cardiovascular Research, and eDepartment of Physiology, 2nd Faculty of Medicine, Charles University, Prague, Czech Republic; fSection of Nephrology, Medical Policlinic, Department of Medicine, University of Bonn, Bonn, and gMax Delbrück Center for Molecular Medicine, Berlin, Germany; hDepartment of Physiology and Biophysics, Federal University of Minas Gerais, Belo Horizonte, Brazil
                Author notes
                *Luděk Červenka, MD, PhD, Department for Experimental Medicine, Institute for Clinical and Experimental Medicine, 1958/9 Vídeňská, CZ–140 00 Prague 4 (Czech Republic), Tel. +420 2 6136 2126, Fax +420 2 4172 1666, E-Mail luce@medicon.cz
                Article
                Publisher ID: 320689 Other ID: Kidney Blood Press Res 2010;33:476–488
                DOI: 10.1159/000320689
                PubMed ID: 21071955
                SO-VID: de79af62-4dab-4640-8d45-917c3284b369
                Copyright © © 2010 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 : 15 June 2010
                Date accepted : 24 August 2010
                Page count
                Figures: 5, References: 43, Pages: 13
                Categories
                Subject: Original Paper

                ScienceOpen disciplines: Cardiovascular Medicine,Nephrology
                Keywords: Mas receptor knockout mice,Two-kidney, one-clip Goldblatt hypertension,Nitric oxide deficiency
                Data availability:
                ScienceOpen disciplines: Cardiovascular Medicine, Nephrology
                Keywords: Mas receptor knockout mice, Two-kidney, one-clip Goldblatt hypertension, Nitric oxide deficiency

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