Angiotensin II for the Treatment of COVID-19–Related Vasodilatory Shock

The Renin-Angiotensin-Aldosterone System in Coronavirus Infection—Current Considerations During the Pandemic

“…[4][5] A second possibility is that the severe alveolar endothelial damage from adult respiratory distress syndrome may disrupt the function of angiotensin-converting enzyme 1, interfering with the hydrolysis of angiotensin I to form angiotensin II. [1][2][3] The resulting deficiency of angiotensin II leads to loss of systemic vascular tone. [2][3] Furthermore, the resulting excess of angiotensin I also aggravates vasoplegia through the enhanced production of nitric oxide and bradykinin.…”

“…[1][2][3] The resulting deficiency of angiotensin II leads to loss of systemic vascular tone. [2][3] Furthermore, the resulting excess of angiotensin I also aggravates vasoplegia through the enhanced production of nitric oxide and bradykinin. [2][3] The possibility therefore exists that vasoplegic shock in severe COVID-19 may be due to dysregulation of the renin-angiotensin-aldosterone system with consequent angiotensin II deficiency, suggesting that exogenous administration of this vasopressor may have a unique role in this clinical scenario.…”

“…The renin-angiotensin-aldosterone system (RAAS) is a complex peptide cascade that has a prominent role in multiple important physiological processes such as vascular tone, vascular permeability, and myocardial remodeling. [1][2][3] The pharmacologic modulation of this system with agents such as angiotensin-converting enzyme inhibitors (ACEI) and angiotensin receptor blockers (ARBS) has resulted in major clinical benefits in the medical management of hypertension and heart failure. 3 Furthermore, the consequences of this pharmacologic blockade of the RAAS in perioperative cardiothoracic and vascular practice has been well-recognized, leading to the emergence of rescue therapies for support of vascular tone.…”

“…[4][5] The severe acute respiratory syndrome coronavirus-2 infects human cells such as alveolar endothelium in the lung by binding to the membrane receptor, angiotensin-converting enzyme 2 (ACE2). [1][2][3] Although the physiologic functions of ACE2 include counteracting the effects of RAAS activation, it also functions as a membrane receptor for the coronavirus. [1][2][3] This binding results in endocytosis of the viral complex with consequent local activation of the RAAS, resulting in acute lung injury that may progress to adult respiratory distress syndrome.…”

“…[1][2][3] Although the physiologic functions of ACE2 include counteracting the effects of RAAS activation, it also functions as a membrane receptor for the coronavirus. [1][2][3] This binding results in endocytosis of the viral complex with consequent local activation of the RAAS, resulting in acute lung injury that may progress to adult respiratory distress syndrome. 1-2 ; 6-7 The purpose of this freestanding editorial is to highlight the considerations concerning the RAAS in patients presenting with severe coronavirus disease 2019 .…”