Srinivasan A, Dhivya P. Dysregulation of renin-angiotensin-aldosterone axis in septic shock: Emerging roles of angiotensin-(1-5) and alamandine. World J Crit Care Med 2026; 15(1): 114670 [DOI: 10.5492/wjccm.v15.i1.114670]
Corresponding Author of This Article
Arunkumaar Srinivasan, Consultant, Department of GI and Renal Critical Care, Apollo Hospital, Greams Lane, Chennai 600006, Tamil Nadu, India. arundec06@gmail.com
Research Domain of This Article
Critical Care Medicine
Article-Type of This Article
Letter to the Editor
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Mar 9, 2026 (publication date) through Mar 3, 2026
Times Cited of This Article
Times Cited (0)
Journal Information of This Article
Publication Name
World Journal of Critical Care Medicine
ISSN
2220-3141
Publisher of This Article
Baishideng Publishing Group Inc, 7041 Koll Center Parkway, Suite 160, Pleasanton, CA 94566, USA
Share the Article
Srinivasan A, Dhivya P. Dysregulation of renin-angiotensin-aldosterone axis in septic shock: Emerging roles of angiotensin-(1-5) and alamandine. World J Crit Care Med 2026; 15(1): 114670 [DOI: 10.5492/wjccm.v15.i1.114670]
World J Crit Care Med. Mar 9, 2026; 15(1): 114670 Published online Mar 9, 2026. doi: 10.5492/wjccm.v15.i1.114670
Dysregulation of renin-angiotensin-aldosterone axis in septic shock: Emerging roles of angiotensin-(1-5) and alamandine
Arunkumaar Srinivasan, Ponnsusamy Dhivya
Arunkumaar Srinivasan, Department of GI and Renal Critical Care, Apollo Hospital, Chennai 600006, Tamil Nadu, India
Ponnsusamy Dhivya, Department of Pediatrics, Sri Lalithambigai Medical College and Hospital, Chennai 600095, Tamil Nadu, India
Co-first authors: Arunkumaar Srinivasan and Ponnsusamy Dhivya.
Author contributions: Srinivasan A and Dhivya P contributed equally in preparing the manuscript as co-first authors.
Conflict-of-interest statement: All authors declare no conflict of interest in publishing the manuscript.
Corresponding author: Arunkumaar Srinivasan, Consultant, Department of GI and Renal Critical Care, Apollo Hospital, Greams Lane, Chennai 600006, Tamil Nadu, India. arundec06@gmail.com
Received: September 25, 2025 Revised: November 21, 2025 Accepted: January 26, 2026 Published online: March 9, 2026 Processing time: 156 Days and 12.8 Hours
Core Tip
Core Tip: Septic shock, as defined by sepsis-3, is a severe form of sepsis marked by high mortality, requiring vasopressors to maintain mean arterial pressure ≥ 65 mmHg and lactate > 2 mmol/L despite fluids. It involves circulatory and metabolic failure. Normally, the renin-angiotensin-aldosterone axis and sympathetic nervous system maintain vascular tone and volume. In septic shock, dysregulation occurs: Reduced angiotensin (Ang)-converting enzyme activity lowers Ang II and blunts vasoconstriction, while counter-regulatory pathways via Ang-converting enzyme 2-Ang-(1–7)-mas receptor promote vasodilation. Emerging metabolites like Ang-(1–5) and alamandine show cardioprotective roles, suggesting therapeutic potential in rebalancing renin-Ang-aldosterone signaling for refractory shock.
