Research output: Contribution to journal/Conference contribution in journal/Contribution to newspaper › Review › Research › peer-review
SARS-CoV-2 and hypertension. / Ravichandran, Briyanth; Grimm, Daniela; Krüger, Marcus et al.
In: Physiological Reports, Vol. 9, No. 11, e14800, 06.2021.Research output: Contribution to journal/Conference contribution in journal/Contribution to newspaper › Review › Research › peer-review
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TY - JOUR
T1 - SARS-CoV-2 and hypertension
AU - Ravichandran, Briyanth
AU - Grimm, Daniela
AU - Krüger, Marcus
AU - Kopp, Sascha
AU - Infanger, Manfred
AU - Wehland, Markus
N1 - Publisher Copyright: © 2021 The Authors. Physiological Reports published by Wiley Periodicals LLC on behalf of The Physiological Society and the American Physiological Society Copyright: Copyright 2021 Elsevier B.V., All rights reserved.
PY - 2021/6
Y1 - 2021/6
N2 - The objective of this review is to give an overview of the pathophysiological effects of the Coronavirus Disease 2019 (COVID-19) in relation to hypertension (HT), with a focus on the Renin–Angiotensin–Aldosterone System (RAAS) and the MAS receptor. HT is a multifactorial disease and a public health burden, as it is a risk factor for diseases like stroke, coronary artery disease, and heart failure, leading to 10.4 million deaths yearly. Blood pressure is regulated by the RAAS. The system consists of two counter-regulatory axes: ACE/ANG-II/AT1R and ACE2/ANG-(1-7)/MAS. The main regulatory protein in balancing the RAAS is angiotensin-converting enzyme 2 (ACE2). The protein also functions as the main mediator of endocytosis of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) into the host cell. SARS-CoV-2 is the cause of COVID-19 and has caused a worldwide pandemic; however, the treatment and prophylaxis of COVID-19 are limited. Several drugs and vaccines are currently being tested in clinical trials with a few already approved by EMA and FDA. HT is a major risk factor regarding the severity and fatality of COVID-19, and the RAAS plays an important role in COVID-19 infection since SARS-CoV-2 can lead to a dysregulation of the system by reducing the ACE2 expression. The exact mechanisms of HT in relation to COVID-19 remain uncertain, and more research is needed for further elucidation.
AB - The objective of this review is to give an overview of the pathophysiological effects of the Coronavirus Disease 2019 (COVID-19) in relation to hypertension (HT), with a focus on the Renin–Angiotensin–Aldosterone System (RAAS) and the MAS receptor. HT is a multifactorial disease and a public health burden, as it is a risk factor for diseases like stroke, coronary artery disease, and heart failure, leading to 10.4 million deaths yearly. Blood pressure is regulated by the RAAS. The system consists of two counter-regulatory axes: ACE/ANG-II/AT1R and ACE2/ANG-(1-7)/MAS. The main regulatory protein in balancing the RAAS is angiotensin-converting enzyme 2 (ACE2). The protein also functions as the main mediator of endocytosis of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) into the host cell. SARS-CoV-2 is the cause of COVID-19 and has caused a worldwide pandemic; however, the treatment and prophylaxis of COVID-19 are limited. Several drugs and vaccines are currently being tested in clinical trials with a few already approved by EMA and FDA. HT is a major risk factor regarding the severity and fatality of COVID-19, and the RAAS plays an important role in COVID-19 infection since SARS-CoV-2 can lead to a dysregulation of the system by reducing the ACE2 expression. The exact mechanisms of HT in relation to COVID-19 remain uncertain, and more research is needed for further elucidation.
KW - COVID-19
KW - hypertension
KW - MAS-receptor
KW - renin–angiotensin–aldosterone system
KW - SARS-CoV-2
UR - http://www.scopus.com/inward/record.url?scp=85107826205&partnerID=8YFLogxK
U2 - 10.14814/phy2.14800
DO - 10.14814/phy2.14800
M3 - Review
C2 - 34121359
AN - SCOPUS:85107826205
VL - 9
JO - Physiological Reports
JF - Physiological Reports
SN - 2051-817X
IS - 11
M1 - e14800
ER -