Norepinephrine and Vasopressin in Hemorrhagic Shock: A Focus on Renal Hemodynamics

During hemorrhagic shock, blood loss causes a fall in blood pressure, decreases cardiac output, and, consequently, O transport. The current guidelines recommend the administration of vasopressors in addition to fluids to maintain arterial pressure when life-threatening hypotension occurs in order to...

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Bibliographic Details
Published in:International journal of molecular sciences Vol. 24; no. 4; p. 4103
Main Authors: Fage, Nicolas, Asfar, Pierre, Radermacher, Peter, Demiselle, Julien
Format: Journal Article
Language:English
Published: Switzerland MDPI AG 01-02-2023
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Summary:During hemorrhagic shock, blood loss causes a fall in blood pressure, decreases cardiac output, and, consequently, O transport. The current guidelines recommend the administration of vasopressors in addition to fluids to maintain arterial pressure when life-threatening hypotension occurs in order to prevent the risk of organ failure, especially acute kidney injury. However, different vasopressors exert variable effects on the kidney, depending on the nature and dose of the substance chosen as follows: Norepinephrine increases mean arterial pressure both via its α-1-mediated vasoconstriction leading to increased systemic vascular resistance and its β1-related increase in cardiac output. Vasopressin, through activation of V1-a receptors, induces vasoconstriction, thus increasing mean arterial pressure. In addition, these vasopressors have the following different effects on renal hemodynamics: Norepinephrine constricts both the afferent and efferent arterioles, whereas vasopressin exerts its vasoconstrictor properties mainly on the efferent arteriole. Therefore, this narrative review discusses the current knowledge of the renal hemodynamic effects of norepinephrine and vasopressin during hemorrhagic shock.
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PMCID: PMC9967703
ISSN:1422-0067
1661-6596
1422-0067
DOI:10.3390/ijms24044103