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      Classic and Nonclassic Renin-Angiotensin Systems in the Critically Ill

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          Abstract

          Classic and nonclassic renin-angiotensin systems (RAS) are 2 sides of an ubiquitous endocrine/paracrine cascade regulating blood pressure and homeostasis. Angiotensin II and angiotensin-converting enzyme (ACE) levels are associated with severity of disease in the critically ill, and are central to the physiology and the pathogenesis of circulatory shock. Angiotensin (1–7) and ACE2 act as an endogenous counterregulatory arm to the angiotensin II/ACE axis. The tissue-based RAS has paracrine effects dissociated from those of the circulating RAS. Exogenous angiotensin II or ACE2 may improve the outcome of septic shock and acute respiratory distress syndrome, respectively.

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          Classical Renin-Angiotensin system in kidney physiology.

          Matthew Sparks, Steven Crowley, Susan Gurley … (2014)
          The renin-angiotensin system has powerful effects in control of the blood pressure and sodium homeostasis. These actions are coordinated through integrated actions in the kidney, cardiovascular system and the central nervous system. Along with its impact on blood pressure, the renin-angiotensin system also influences a range of processes from inflammation and immune responses to longevity. Here, we review the actions of the "classical" renin-angiotensin system, whereby the substrate protein angiotensinogen is processed in a two-step reaction by renin and angiotensin converting enzyme, resulting in the sequential generation of angiotensin I and angiotensin II, the major biologically active renin-angiotensin system peptide, which exerts its actions via type 1 and type 2 angiotensin receptors. In recent years, several new enzymes, peptides, and receptors related to the renin-angiotensin system have been identified, manifesting a complexity that was previously unappreciated. While the functions of these alternative pathways will be reviewed elsewhere in this journal, our focus here is on the physiological role of components of the "classical" renin-angiotensin system, with an emphasis on new developments and modern concepts.
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            Renal ACE2 expression in human kidney disease.

            A Lely, Doorlene van Tienoven, G. Navis … (2004)
            Angiotensin-converting enzyme 2 (ACE2) is a recently discovered homologue of angiotensin-converting enzyme (ACE) that is thought to counterbalance ACE. ACE2 cleaves angiotensin I and angiotensin II into the inactive angiotensin 1-9, and the vasodilator and anti-proliferative angiotensin 1-7, respectively. ACE2 is known to be present in human kidney, but no data on renal disease are available to date. Renal biopsies from 58 patients with diverse primary and secondary renal diseases were studied (hypertensive nephropathy n = 5, IgA glomerulopathy n = 8, minimal change nephropathy n = 7, diabetic nephropathy n = 8, focal glomerulosclerosis n = 5, vasculitis n = 7, and membranous glomerulopathy n = 18) in addition to 17 renal transplants and 18 samples from normal renal tissue. Immunohistochemical staining for ACE2 was scored semi-quantitatively. In control kidneys, ACE2 was present in tubular and glomerular epithelium and in vascular smooth muscle cells and the endothelium of interlobular arteries. In all primary and secondary renal diseases, and renal transplants, neo-expression of ACE2 was found in glomerular and peritubular capillary endothelium. There were no differences between the various renal disorders, or between acute and chronic rejection and control transplants. ACE inhibitor treatment did not alter ACE2 expression. In primary and secondary renal disease, and in transplanted kidneys, neo-expression of ACE2 occurs in glomerular and peritubular capillary endothelium. Further studies should elucidate the possible protective mechanisms involved in the de novo expression of ACE2 in renal disease. Copyright (c) 2004 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
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              Liver angiotensinogen is the primary source of renal angiotensin II.

              Iekuni Ichikawa, A Shimizu, Akihiko Saito … (2012)
              Angiotensin II content in the kidney is much higher than in the plasma, and it increases more in kidney diseases through an uncertain mechanism. Because the kidney abundantly expresses angiotensinogen mRNA, transcriptional dysregulation of angiotensinogen within the kidney is one potential cause of increased renal angiotensin II in the setting of disease. Here, we observed that kidney-specific angiotensinogen knockout mice had levels of renal angiotensinogen protein and angiotensin II that were similar to those levels of control mice. In contrast, liver-specific knockout of angiotensinogen nearly abolished plasma and renal angiotensinogen protein and renal tissue angiotensin II. Immunohistochemical analysis in mosaic proximal tubules of megalin knockout mice revealed that angiotensinogen protein was incorporated selectively in megalin-intact cells of the proximal tubule, indicating that the proximal tubule reabsorbs filtered angiotensinogen through megalin. Disruption of the filtration barrier in a transgenic mouse model of podocyte-selective injury increased renal angiotensin II content and markedly increased both tubular and urinary angiotensinogen protein without an increase in renal renin activity, supporting the dependency of renal angiotensin II generation on filtered angiotensinogen. Taken together, these data suggest that liver-derived angiotensinogen is the primary source of renal angiotensinogen protein and angiotensin II. Furthermore, an abnormal increase in the permeability of the glomerular capillary wall to angiotensinogen, which characterizes proteinuric kidney diseases, enhances the synthesis of renal angiotensin II.
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                Author and article information

                Contributors
                Laurent Bitker
                Journal
                Journal ID (nlm-ta): Crit Care Clin
                Journal ID (iso-abbrev): Crit Care Clin
                Title: Critical Care Clinics
                Publisher: Elsevier Inc.
                ISSN (Print): 0749-0704
                ISSN (Electronic): 1557-8232
                Publication date PMC-release: 28 January 2019
                Publication date (Print): April 2019
                Publication date (Electronic): 28 January 2019
                Volume: 35
                Issue: 2
                Pages: 213-227
                Affiliations
                [a ]Department of Intensive Care, ICU Research Office, Austin Hospital, 145 Studley Road, Heidelberg, Victoria 3084, Australia
                [b ]Department of Medicine, University of Melbourne, Austin Health, Austin Hospital, 145 Studley Road, Heidelberg, Victoria 3084, Australia
                Author notes
                [∗ ]Corresponding author. laurent.bitker@ 123456austin.org.au
                Article
                Publisher ID: S0749-0704(18)30770-X
                DOI: 10.1016/j.ccc.2018.11.002
                PMC ID: 7125612
                PubMed ID: 30784605
                SO-VID: 490eae4f-aa6d-41b2-866d-a9f7c11d31f4
                Copyright © © 2018 Elsevier Inc. All rights reserved.
                License:

                Since January 2020 Elsevier has created a COVID-19 resource centre with free information in English and Mandarin on the novel coronavirus COVID-19. The COVID-19 resource centre is hosted on Elsevier Connect, the company's public news and information website. Elsevier hereby grants permission to make all its COVID-19-related research that is available on the COVID-19 resource centre - including this research content - immediately available in PubMed Central and other publicly funded repositories, such as the WHO COVID database with rights for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for free by Elsevier for as long as the COVID-19 resource centre remains active.

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                Subject: Article

                Keywords: acute kidney injury,acute respiratory distress syndrome,angiotensin,angiotensin-converting enzyme,sepsis,inflammation,septic shock,renin
                Data availability:
                Keywords: acute kidney injury, acute respiratory distress syndrome, angiotensin, angiotensin-converting enzyme, sepsis, inflammation, septic shock, renin

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