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Part of the book series: Annual Update in Intensive Care and Emergency Medicine 2015 ((AUICEM,volume 2015))

Abstract

Systemic vasodilatation and arterial hypotension are landmarks of septic shock. Whenever fluid resuscitation fails to restore arterial blood pressure and tissue perfusion, vasopressors agents are necessary [1]. Norepinephrine, a strong α-adrenergic agonist, is the standard vasopressor to treat septic shock-induced hypotension [1]. Adrenergic vasopressors have been associated with several detrimental effects, including organ dysfunction and increased mortality [2, 3]. Therefore, alternative agents have been proposed, yet with disappointing results so far [4].

The renin-angiotensin system (RAS) provides an important physiologic mechanism to prevent systemic hypotension under hypovolemic conditions, such as unresuscitated septic shock [5]. In addition to its classical hemodynamic function of regulating arterial blood pressure, angiotensin II plays a key role in several biological processes, including cell growth, apoptosis, inflammatory response, and coagulation. It may also affect mitochondrial function [6, 7].

This review briefly discusses the main physiological functions of the RAS, and presents recent evidence suggesting a role for exogenous angiotensin II administration as a vasopressor in septic shock.

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Corrêa, T.D., Takala, J., Jakob, S.M. (2015). Angiotensin II in Septic Shock. In: Vincent, JL. (eds) Annual Update in Intensive Care and Emergency Medicine 2015. Annual Update in Intensive Care and Emergency Medicine 2015, vol 2015. Springer, Cham. https://doi.org/10.1007/978-3-319-13761-2_10

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  • DOI: https://doi.org/10.1007/978-3-319-13761-2_10

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