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      View of the Renin-Angiotensin System in Acute Kidney Injury Induced by Renal Ischemia-Reperfusion Injury

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          Abstract

          Renal ischemia-reperfusion injury (RIRI) is a sequence of complicated events that is defined as a reduction of the blood supply followed by reperfusion. RIRI is the leading cause of acute kidney injury (AKI). Among the diverse mediators that take part in RIRI-induced AKI, the renin-angiotensin system (RAS) plays an important role via conventional (angiotensinogen, renin, angiotensin-converting enzyme (ACE), angiotensin (Ang) II, and Ang II type 1 receptor (AT 1R)) and nonconventional (ACE2, Ang 1-7, Ang 1-9, AT 2 receptor (AT 2R), and Mas receptor (MasR)) axes. RIRI alters the balance of both axes so that RAS can affect RIRI-induced AKI. In overall, the alteration of Ang II/AT 1R and AKI by RIRI is important to consider. This review has looked for the effects and interactions of RAS activities during RIRI conditions.

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          A novel angiotensin-converting enzyme-related carboxypeptidase (ACE2) converts angiotensin I to angiotensin 1-9.

          Mary Donoghue, Frank Hsieh, Elizabeth Baronas … (2000)
          ACE2, the first known human homologue of angiotensin-converting enzyme (ACE), was identified from 5' sequencing of a human heart failure ventricle cDNA library. ACE2 has an apparent signal peptide, a single metalloprotease active site, and a transmembrane domain. The metalloprotease catalytic domains of ACE2 and ACE are 42% identical, and comparison of the genomic structures indicates that the two genes arose through duplication. In contrast to the more ubiquitous ACE, ACE2 transcripts are found only in heart, kidney, and testis of 23 human tissues examined. Immunohistochemistry shows ACE2 protein predominantly in the endothelium of coronary and intrarenal vessels and in renal tubular epithelium. Active ACE2 enzyme is secreted from transfected cells by cleavage N-terminal to the transmembrane domain. Recombinant ACE2 hydrolyzes the carboxy terminal leucine from angiotensin I to generate angiotensin 1-9, which is converted to smaller angiotensin peptides by ACE in vitro and by cardiomyocytes in culture. ACE2 can also cleave des-Arg bradykinin and neurotensin but not bradykinin or 15 other vasoactive and hormonal peptides tested. ACE2 is not inhibited by lisinopril or captopril. The organ- and cell-specific expression of ACE2 and its unique cleavage of key vasoactive peptides suggest an essential role for ACE2 in the local renin-angiotensin system of the heart and kidney. The full text of this article is available at http://www. circresaha.org.
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            Pathophysiology of acute kidney injury.

            David P Basile, Melissa Anderson, Timothy A. Sutton (2012)
            Acute kidney injury (AKI) is the leading cause of nephrology consultation and is associated with high mortality rates. The primary causes of AKI include ischemia, hypoxia, or nephrotoxicity. An underlying feature is a rapid decline in glomerular filtration rate (GFR) usually associated with decreases in renal blood flow. Inflammation represents an important additional component of AKI leading to the extension phase of injury, which may be associated with insensitivity to vasodilator therapy. It is suggested that targeting the extension phase represents an area potential of treatment with the greatest possible impact. The underlying basis of renal injury appears to be impaired energetics of the highly metabolically active nephron segments (i.e., proximal tubules and thick ascending limb) in the renal outer medulla, which can trigger conversion from transient hypoxia to intrinsic renal failure. Injury to kidney cells can be lethal or sublethal. Sublethal injury represents an important component in AKI, as it may profoundly influence GFR and renal blood flow. The nature of the recovery response is mediated by the degree to which sublethal cells can restore normal function and promote regeneration. The successful recovery from AKI depends on the degree to which these repair processes ensue and these may be compromised in elderly or chronic kidney disease (CKD) patients. Recent data suggest that AKI represents a potential link to CKD in surviving patients. Finally, earlier diagnosis of AKI represents an important area in treating patients with AKI that has spawned increased awareness of the potential that biomarkers of AKI may play in the future. © 2012 American Physiological Society. Compr Physiol 2:1303-1353, 2012.
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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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                Author and article information

                Contributors
                Mehdi Nematbakhsh:
                ORCID: https://orcid.org/0000-0002-9565-9187
                Journal
                Journal ID (nlm-ta): J Renin Angiotensin Aldosterone Syst
                Journal ID (iso-abbrev): J Renin Angiotensin Aldosterone Syst
                Journal ID (publisher-id): JRAAS
                Title: Journal of the Renin-Angiotensin-Aldosterone System: JRAAS
                Publisher: Hindawi
                ISSN (Print): 1470-3203
                ISSN (Electronic): 1752-8976
                Publication date Collection: 2022
                Publication date (Electronic): 22 October 2022
                Volume: 2022
                Electronic Location Identifier: 9800838
                Affiliations
                1Department of Physiology, Behbahan Faculty of Medical Sciences, Behbahan, Iran
                2Department of Physiology, Faculty of Medicine, Ilam University of Medical Sciences, Ilam, Iran
                3Water & Electrolytes Research Center, Isfahan University of Medical Sciences, Isfahan, Iran
                Author notes

                Academic Editor: Meili Sun

                Author information
                https://orcid.org/0000-0002-1512-7333
                https://orcid.org/0000-0002-1342-553X
                https://orcid.org/0000-0002-9565-9187
                Article
                DOI: 10.1155/2022/9800838
                PMC ID: 9617735
                PubMed ID: 36320442
                SO-VID: 84557308-7dc8-4678-8182-e2bac8a47030
                Copyright © Copyright © 2022 Farzaneh Karimi et al.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 3 July 2022
                Date revision received : 6 October 2022
                Date accepted : 12 October 2022
                Funding
                Funded by: Behbahan Faculty of Medical Sciences
                Award ID: 401024
                Categories
                Subject: Review Article

                Data availability:

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