Angiotensin in Critical Care

Hall, Anna; Busse, Laurence W.; Ostermann, Marlies

doi:10.1007/978-3-319-73670-9_10

Cited by 8 publications

(17 citation statements)

References 45 publications

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“…The renin-angiotensin system (RAS) is a complex pathway responsible for maintaining arterial blood pressure and volume homeostasis. 77 Although a comprehensive review of this pathway as well as all of the physiologic functions is beyond the scope of this article, a concise review of the proposed mechanisms of ATII as a vasoconstrictor is discussed here. 77 Angiotensin II, an octapeptide, predominantly exerts direct arterial vasoconstriction by binding to the angiotensin (AT)-1 receptors located on the vascular smooth muscle.…”

Section: Background and Pharmacologymentioning

confidence: 99%

“…77 Although a comprehensive review of this pathway as well as all of the physiologic functions is beyond the scope of this article, a concise review of the proposed mechanisms of ATII as a vasoconstrictor is discussed here. 77 Angiotensin II, an octapeptide, predominantly exerts direct arterial vasoconstriction by binding to the angiotensin (AT)-1 receptors located on the vascular smooth muscle. 77 Other ATII-mediated cardiovascular physiologic effects through the AT-1 receptors potentially impacting arterial pressure homeostasis include the secretion of NE, vasopressin, and adrenocorticotropic hormone, as well as water and sodium reabsorption.…”

Section: Background and Pharmacologymentioning

confidence: 99%

“…77 Angiotensin II, an octapeptide, predominantly exerts direct arterial vasoconstriction by binding to the angiotensin (AT)-1 receptors located on the vascular smooth muscle. 77 Other ATII-mediated cardiovascular physiologic effects through the AT-1 receptors potentially impacting arterial pressure homeostasis include the secretion of NE, vasopressin, and adrenocorticotropic hormone, as well as water and sodium reabsorption. 77 Although vasodilation and reduced systemic vascular resistance from AT-2 receptor stimulation from ATII may counteract the agonistic vascular effects of AT-1 receptors, AT-2 receptors were associated with adrenal catecholamine secretion.…”

Section: Background and Pharmacologymentioning

confidence: 99%

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Catecholamine Vasopressor Support Sparing Strategies in Vasodilatory Shock

et al. 2019

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Shock syndromes are associated with unacceptably high rates of mortality in critically ill patients despite advances in therapeutic options. Vasodilatory shock is the most common type encountered in the intensive care unit. It is manifested by cardiovascular failure, peripheral vasodilatation, and arterial hypotension leading to tissue hypoperfusion and organ failure. Hemodynamic support is typically initiated with fluid resuscitation strategies and administration of adrenergic vasopressor agents in nonresponsive patients to restore arterial pressure with subsequent adequate organ reperfusion. Unfortunately, high catecholamine dosing requirements may be necessary to achieve targeted hemodynamic goals that may increase the risk of vasopressor‐induced adverse events. The purpose of this article is to review the clinical efficacy and safety data and potential role in therapy for catecholamine‐sparing agents in vasodilatory shock. Adjunctive therapeutic options to reduce vasoactive support requirements without compromising arterial pressure include arginine vasopressin and analogs, corticosteroids, midodrine, methylene blue, and angiotensin II. Although concomitant vasopressin and corticosteroids have a more defined role in evidence‐based guidelines for managing shock, clinicians may consider other potential catecholamine‐sparing agents.

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Section: Background and Pharmacologymentioning

confidence: 99%

Section: Background and Pharmacologymentioning

confidence: 99%

Section: Background and Pharmacologymentioning

confidence: 99%

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Catecholamine Vasopressor Support Sparing Strategies in Vasodilatory Shock

et al. 2019

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“…Angiotensin II can also bind the angiotensin receptor type 2 leading to vasodilation and a counterbalancing of the vasoconstrictive effects of AT1 augmentation in some vascular beds. 29 Despite these seemingly competing receptor effects on the vasculature, when exogenously administered, angiotensin II increases blood pressure. The effects of angiotensin II compared with placebo were investigated in the Angiotensin II for the Treatment of High-Output Shock (ATHOS-3) study.…”

Section: Adrs Of Angiotensin II and Risk Mitigationmentioning

confidence: 99%

“…Utilizing these therapies in patients who are not predicted to respond (whether a hemodynamic response, mortality benefit, or other definition) only subjects them to the potential for harm without the purported benefits. Reviews devoted to this topic exist in the literature, 28,29,46,47 but some major points and nuances deserve discussion.…”

Section: Strategies To Minimize Adr Risk For Both Agentsmentioning

confidence: 99%

Safe Use of Vasopressin and Angiotensin II for Patients with Circulatory Shock

2018

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Circulatory shock is a medical emergency that requires rapid intervention to optimize patient outcomes. Although catecholamine vasopressors are considered life‐sustaining therapy, they are associated with adverse reactions, and vasopressin and angiotensin II may be used to minimize these adverse effects. However, vasopressin and angiotensin II are also associated with adverse reactions that must be known to the clinician to mitigate risk for patients. This review focuses on the known adverse drug effects of vasopressin and angiotensin II while offering potential solutions to minimize harm with these agents. Future directions with vasoactive medication safety including optimization of the electronic medical record, clinical decision support, prediction analytics, and precision medicine for patients with circulatory shock are also discussed.

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Role of ACE 2 and Vitamin D: The Two Players in Global Fight against COVID-19 Pandemic

Behl

Shah

Kaur

et al. 2021

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The global pandemic of coronavirus disease 2019 (COVID-19) has spread across the borders, gaining attention from both health care professional and researchers to understand the mode of entry and actions induced by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), its causative agent in the human body. The role of angiotensin-converting enzyme–2 (ACE2) in facilitating the entry of the virus in the host cell by binding to it is similar to SARS-CoV-1, the causative agent for severe acute respiratory syndrome (SARS) which emerged in 2003. Besides the role of ACE2 as a molecular target for the virus, the review displays the potential benefits of ACE2 enzyme and various agents that modify its activity in curbing the effects of the deadly virus, thus unfolding a dual character of ACE2 in the current pandemic. As evident by the differences in the susceptibility toward viral infection in children and geriatric population, it must be noted that the older population has limited ACE2 levels and greater infection risk, whereas the situation is reversed in the case of the pediatric population, demonstrating the defensive character of ACE2 in the latter, despite acting as receptor target for SARS-CoV-2. Also, the upregulation of ACE2 levels by estrogen has indicated greater resistance to infection in females than in the male human population. ACE2 is a carboxypeptidase, which degrades angiotensin II and counteracts its actions to protect against cardiovascular risks associated with the virus. Another contribution of this enzyme is supported by the role of circulating soluble ACE2, which acts as a receptor to bind the virus but does not mediate its actions, therefore blocking its interaction to membrane-bound ACE2 receptors. The review also shares the enhanced risks of developing COVID-19 infection by using ACE inhibitors and ARBs. However, both these agents have been reported to upregulate ACE2 levels; yet, adequate evidence regarding their role is quite inconsistent in human studies. Furthermore, the role of vitamin D has been highlighted in regulating the immune system of the body through renin-angiotensin-aldosterone system (RAAS) inhibition, by downregulating host cell receptor expression to prevent virus attachment. Besides, vitamin D also acts through several other mechanisms like upregulating antimicrobial peptides, fighting against the proinflammatory milieu created by the invading virus, and interfering with the viral replication cycle as well as calcitriol-mediated blockage of CREB protein. Hypovitaminosis D is attributed to elevated risks of acute respiratory distress syndrome (ARDS), lung damage, and cardiovascular disorders, further increasing the severity of COVID-19 infection.

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Angiotensin in Critical Care

Cited by 8 publications

References 45 publications

Catecholamine Vasopressor Support Sparing Strategies in Vasodilatory Shock

Catecholamine Vasopressor Support Sparing Strategies in Vasodilatory Shock

Safe Use of Vasopressin and Angiotensin II for Patients with Circulatory Shock

Role of ACE 2 and Vitamin D: The Two Players in Global Fight against COVID-19 Pandemic

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