SARS‐CoV‐2 and hypertension

Ravichandran, Briyanth; Grimm, Daniela; Krüger, Marcus; Kopp, Sascha; Infanger, Manfred; Wehland, Markus

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/AT(1)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.