Mohammad Asgharzadeh
1 
, Abdolhassan Kazemi
2, Behroz Mahdavipoor
3, Vahid Asgharzadeh
4, Zahra Taghinejad
2, Amirali Mirmazhary
5, Amirhossein Samadikafil
6, MirReza Valiollahzadeh
7, Jalil Rashedi
8, Fariba Pashazadeh
9, Nasrin Abolhasanpour
9* 1 Biotechnology Research Center and Faculty of Paramedicine, Tabriz University of Medical Sciences, Tabriz, Iran
2 Medical Philosophy and History Research Center, Tabriz University of Medical Sciences, Tabriz, Iran
3 Department of Laboratory Sciences, Faculty of Paramedicine, Tabriz University of Medical sciences, Tabriz, Iran
4 Student Research Committee, Tabriz University of Medical sciences, Tabriz, Iran
5 Infectious and Tropical Diseases Research Center, Tabriz University of Medical sciences, Tabriz, Iran
6 Drug Applied Research Center, Tabriz University of Medical sciences, Tabriz, Iran
7 Hematology and Oncology Research Center, Tabriz University of Medical sciences, Tabriz, Iran
8 Tuberculosis and Lung Diseases Research Center, Tabriz University of Medical sciences, Tabriz, Iran
9 Research Center for Evidence-based Medicine, Iranian EBM Centre: A Joanna Briggs Institute (JBI) Centre of Excellence, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran
Abstract
Chinese authorities reported the first human-to-animal SARS-CoV-2 transmission in late 2019. The virus then quickly spread from person to person throughout the world and increased the mortality rate of those with underlying illnesses, particularly hypertension. After attaching the virus to a special receptor, that is, angiotensin-converting enzyme-2 (ACE2), ACE2 degrades angiotensin 2 (Ang2). Ang2 as a modulator of blood pressure and a vasoconstrictor plays an adverse regulatory role in the renin-angiotensin system (RAS). Additionally, it changes Ang2 into Ang1-7, which functions as an antioxidant and an anti-inflammatory factor. Infection with SARSCoV-2 lowers ACE2 levels in hypertensive patients because the virus binds to the blood vessel, preventing Ang II degradation. As a result, complications related to hypertension increase, and the pumping of blood from the lungs to the left atrium decreases. Additionally, there is a decrease in the final product, Ang1-7, and the concomitant anti-inflammatory action is lost. The virus grows, multiplies, damages lung cells, causing inflammation in immune cells and cytokines and expanding lung tissue. This ultimately leads to lung injury, a decline in the oxygen supply, and death. The management of hypertensive patients can prevent infection in this population and reduce mortality with proper oxygen therapy and probably exogenous ACE2 supplementation.