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Updated: Nov 2, 2025

Live Imaging and Quantification of Viral Infection in K18 hACE2 Transgenic Mice Using Reporter-Expressing Recombinant SARS-CoV-2
Published on: November 5, 2021
SARS-CoV-2 and hypertension
Briyanth Ravichandran1, Daniela Grimm1,2, Marcus Krüger2
1Department of Biomedicine, Aarhus University, Aarhus, Denmark.
Insights
Hypertension (HT) exacerbates COVID-19 severity by disrupting the Renin-Angiotensin-Aldosterone System (RAAS). SARS-CoV-2 infection downregulates ACE2, a key RAAS regulator, impacting blood pressure and disease outcomes.
Area of Science:
- Cardiovascular Medicine
- Infectious Diseases
- Molecular Biology
Background:
- Hypertension (HT) is a major global health burden and risk factor for cardiovascular diseases, contributing to millions of deaths annually.
- The Renin-Angiotensin-Aldosterone System (RAAS) is crucial for blood pressure regulation, involving counter-regulatory axes.
- Angiotensin-converting enzyme 2 (ACE2) plays a vital role in balancing the RAAS and serves as the entry receptor for SARS-CoV-2.
Purpose of the Study:
- To review the pathophysiological effects of COVID-19 in relation to hypertension.
- To focus on the role of the RAAS and the MAS receptor in COVID-19 and HT.
- To elucidate the mechanisms linking SARS-CoV-2 infection, RAAS dysregulation, and HT severity.
Main Methods:
- Literature review of existing studies on COVID-19, hypertension, and the RAAS.
- Analysis of the interaction between SARS-CoV-2 and the ACE2 receptor.
- Examination of the impact of SARS-CoV-2 on RAAS components and function.
Main Results:
- Hypertension is a significant risk factor for severe COVID-19 outcomes and mortality.
- SARS-CoV-2 infection can lead to the downregulation of ACE2, causing RAAS dysregulation.
- The interaction between SARS-CoV-2 and ACE2 impacts cardiovascular function and disease progression.
Conclusions:
- The RAAS plays a critical role in the pathophysiology of COVID-19, particularly in hypertensive patients.
- Dysregulation of the RAAS by SARS-CoV-2 contributes to increased disease severity.
- Further research is essential to fully understand the complex interplay between COVID-19, hypertension, and the RAAS.
Abstract:
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/AT1 R 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.
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