Angiotensin II Modulation in Shock and Sepsis Management

Summary

Shock and sepsis remain leading causes of mortality in intensive care worldwide, driven by profound vasodilation, endothelial dysfunction and dysregulated host responses. Angiotensin II, a principal effector hormone of the renin-angiotensin system, exerts potent vasoconstrictive and pro-inflammatory effects that can restore vascular tone and support organ perfusion in catecholamine-refractory states. In distributive shock, endogenous angiotensin II levels are often insufficient relative to vasodilatory burden, prompting the therapeutic use of exogenous angiotensin II infusions. Clinical experience demonstrates that angiotensin II can reduce the requirement for conventional vasopressors such as norepinephrine, improve arterial pressure rapidly and, in certain subgroups, translate into improved survival. Beyond its vasopressor actions, angiotensin II may influence renal function via modulation of glomerular filtration, and affect microcirculatory flow through interactions with inflammatory mediators. Its integration into multimodal resuscitation strategies highlights a shift towards personalised haemodynamic management, guided by biomarker assessment of renin-angiotensin axis activity. Nevertheless, optimisation of dosing, timing and patient selection remains under active investigation, balancing the risks of excessive vasoconstriction, thrombosis and renal ischaemia.

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Angiotensin II Modulation in Shock and Sepsis Management publication trend

The graph below shows the total number of articles in angiotensin ii modulation in shock and sepsis management across all publications each year (not limited to Nature Index journals).

Technical terms

Angiotensin II: A peptide hormone that induces vasoconstriction and raises blood pressure.

Renin-angiotensin system (RAS): A hormonal cascade regulating vascular tone, fluid balance and electrolyte homeostasis.

Vasodilatory shock: A state of critical hypotension due to widespread blood vessel dilation and reduced responsiveness to vasoconstrictors.

Norepinephrine-equivalent dose (NED): A standardised measure of vasopressor support intensity, expressed relative to norepinephrine potency.

Mean arterial pressure (MAP): The average arterial pressure during a cardiac cycle, reflecting organ perfusion pressure.

Acute respiratory distress syndrome (ARDS): A severe form of lung injury characterised by hypoxaemia, diffuse inflammation and impaired gas exchange.

References

  1. Initiating angiotensin II at lower vasopressor doses in vasodilatory shock: an exploratory post-hoc analysis of the ATHOS-3 clinical trial. Critical Care (2023).
  2. Angiotensin II treatment is associated with improved oxygenation in ARDS patients with refractory vasodilatory shock. Annals of Intensive Care (2023).
  3. Angiotensin I and angiotensin II concentrations and their ratio in catecholamine-resistant vasodilatory shock. Critical Care (2020).

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