Role of renin-angiotensin-aldosterone system in the interaction with coronavirus SARS-CoV-2 and in the development of strategies for prevention and treatment of new coronavirus infection (COVID-19)

Abstract

The 2019 coronavirus pandemic (COVID-19), due to the new SARS-CoV-2 virus, represents the greatest global public health crisis and an unprecedented challenge to find effective ways to prevent and treat. In the active phase of a pandemic, early results allow these preventive measures to be implemented on a scale compatible with the pandemic. If the results are convincing, their value will be difficult to overestimate, since additional one or two outbreaks of this infection are expected. Clinical data is emerging rapidly from a large number of people afflicted with SARS-CoV-2, which should provide clinicians with accurate evidence of the effectiveness of different preventive and treatment methods. In particular, an active search is underway for cellular mechanisms that SARS-CoV-2 uses to penetrate tissues. These include information about the receptor of the angiotensin-converting enzyme receptor (ACE 2). SARS-CoV-2, a single-stranded envelope RNA virus, attaches to cells via a viral spike (S) protein that binds to the ACE 2. After binding to the receptor, the viral particle uses the receptors of the host cell and endosomes to enter the cells. Human type transmembrane serine protease 2 (TMPRSS 2) facilitates penetration into the cell via protein S. Once inside the cell, viral polyproteins are synthesized that encode the replicate transcriptase complex. The virus then synthesizes RNA through its RNA-dependent RNA polymerase. Structural proteins are synthesized leading to the completion of the assembly and release of viral particles. These stages of the virus life cycle provide potential targets for drug therapy. Current clinical and scientific data do not support discontinuation of ACE inhibitors or angiotensin receptor blockers in patients with COVID-19, and an ongoing discussion is addressed in this review.

Aterosclerosis, Cardiovascular Disorders And Covid-19: Comorbid Pathogenesis

“…In this review we discuss possible mechanisms of cardiovascular injury in COVID-19, listed in Table 1. as the consequence of COVID-19-induced myocarditis Endothelial dysfunction and coagulopathy [4,14,15] A mismatch between myocardial oxygen supply and demand caused by cardiac overstrain as a compensatory response to hypoxia [12] Systemic inflammatory response, which can results in cytokine storm and hemodynamic shock [7,16] Renin-angiotensin-aldosterone system dysfunction [2,17,18]…”

Mechanisms of Damage to the Cardiovascular System in COVID-19

“…Вопрос о том, должны ли пациенты с COVID-19 и артериальной гипертензией, принимающие ингибиторы АПФ или блокаторы рецепторов ангиотензина, переходить на другое антигипертензивное лекарственное средство, остается спорным. Достаточно подробно роль ренин-ангиотензин-альдостероновой системы при SARS-CoV-2 описана военно-медицинскими специалистами Санкт-Петербурга [21].…”

Coronavirus Infection an Obese Patient (Literature Review)

“…Одной из причин повышенного риска последствий КВИ при ОЖ является активность ангиотензинпревращающего фермента 2 (ACE2) [8,9]. Установлено, что при избыточном весе активируется экспрессия участков генов, ответственных за образование белка ACE 2 [10,11].…”