Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/34339
Title: The alternative renin-angiotensin system in critically ill patients: pathophysiology and therapeutic implications.
Austin Authors: Garcia, Bruno;Zarbock, Alexander;Bellomo, Rinaldo ;Legrand, Matthieu
Affiliation: Department of Anesthesia and Peri-Operative Care, Division of Critical Care Medicine, University of California, San Francisco (UCSF), San Francisco, CA, USA.;Department of Intensive Care, Centre Hospitalier Universitaire de Lille, Lille, France.;Experimental Laboratory of the Department of Intensive Care, Université Libre de Bruxelles, Brussels, Belgium.
Department of Anesthesiology, Intensive Care and Pain Medicine, University Hospital of Münster, Münster, Germany.
Intensive Care
Department of Anesthesia and Peri-Operative Care, Division of Critical Care Medicine, University of California, San Francisco (UCSF), San Francisco, CA, USA.
Australian and New Zealand Intensive Care Research Centre, Monash University, Melbourne, Australia.;Department of Critical Care, Melbourne Medical School, University of Melbourne, Melbourne, VIC, Australia.
Issue Date: 20-Nov-2023
Date: 2023
Publication information: Critical Care (London, England) 2023-11-20; 27(1)
Abstract: The renin-angiotensin system (RAS) plays a crucial role in regulating blood pressure and the cardio-renal system. The classical RAS, mainly mediated by angiotensin I, angiotensin-converting enzyme, and angiotensin II, has been reported to be altered in critically ill patients, such as those in vasodilatory shock. However, recent research has highlighted the role of some components of the counterregulatory axis of the classical RAS, termed the alternative RAS, such as angiotensin-converting Enzyme 2 (ACE2) and angiotensin-(1-7), or peptidases which can modulate the RAS like dipeptidyl-peptidase 3, in many critical situations. In cases of shock, dipeptidyl-peptidase 3, an enzyme involved in the degradation of angiotensin and opioid peptides, has been associated with acute kidney injury and mortality and preclinical studies have tested its neutralization. Angiotensin-(1-7) has been shown to prevent septic shock development and improve outcomes in experimental models of sepsis. In the context of experimental acute lung injury, ACE2 activity has demonstrated a protective role, and its inactivation has been associated with worsened lung function, leading to the use of active recombinant human ACE2, in preclinical and human studies. Angiotensin-(1-7) has been tested in experimental models of acute lung injury and in a recent randomized controlled trial for patients with COVID-19 related hypoxemia. Overall, the alternative RAS appears to have a role in the pathogenesis of disease in critically ill patients, and modulation of the alternative RAS may improve outcomes. Here, we review the available evidence regarding the methods of analysis of the RAS, pathophysiological disturbances of this system, and discuss how therapeutic manipulation may improve outcomes in the critically ill.
URI: https://ahro.austin.org.au/austinjspui/handle/1/34339
DOI: 10.1186/s13054-023-04739-5
ORCID: 
Journal: Critical Care (London, England)
Start page: 453
PubMed URL: 37986086
ISSN: 1466-609X
Type: Journal Article
Subjects: Acute kidney injury
Acute lung injury
Acute respiratory distress syndrome
Angiotensin II
Angiotensin-(1–7)
Angiotensin-converting enzyme 2
Dipeptidyl-peptidase 3
Shock
Renin-Angiotensin System/physiology
Critical Illness/therapy
Angiotensin II/metabolism
Appears in Collections:Journal articles

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