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Increased blood angiotensin converting enzyme 2 activity in critically ill COVID-19 patients

ABSTRACT: Pharmacological blockade of the renin–angiotensin–aldosterone system (RAAS) with angiotensin-converting enzyme (ACE)-inhibitors and angiotensin receptor blockers (ARBs) are cornerstone treatments in several cardiovascular disease entities [1]. The RAAS is a central regulator of blood pressure, consisting of two counterregulatory pathways, commonly described as classical and nonclassical, respectively [1]. The main effect of classical RAAS activation is the generation of angiotensin (Ang)-II by ACE [1]. In contrast, non-classical RAAS activation results in cleavage of Ang-II by angiotensin converting enzyme-2 (ACE2) to form angiotensin 1–7, which directly counteracts the effects of classical RAAS activation [1]. Critically ill #COVID19 patients display markedly increased alternative angiotensin pathway activity compared to healthy controls, reflected by increased blood ACE2 levels as well as decreased angiotensin-II and enhanced angiotensin-1–7 formationhttps://bit.ly/2MU1z4z

PROVIDER: S-EPMC7848790 | BioStudies |

REPOSITORIES: biostudies

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