Renin-angiotensin-aldosterone system in new coronavirus infection 2019

Abstract

The new coronavirus infection (COVID-19) is a serious threat to humanity. Although its pathogenesis has not been fully studied, angiotensin-converting enzyme 2 (ACE 2) has recently been identified as a receptor for entry into the cell of the coronavirus SARS-CoV-2, thereby contributing to the spread of infection in the body. The goal of the review was to study the significance of the renin-angiotensin-aldosterone system (RAAS) in the pathogenesis of the action of the coronavirus SARS-CoV-2, the function and regulation of ACE 2, and the effects of RAAS inhibitors in cardiovascular diseases. ACE 2 promotes the transformation of angiotensin (AT) I into AT 1–7, which have a number of beneficial effects on the state of endothelium and cardiomyocytes (vasodilation, inhibition of cell growth, inhibition of cell proliferation and inhibition of cardiomyocyte hypertrophy). SARS-CoV-2 virus, in addition to interaction with ACE 2 on the surface cells in the lungs and vascular wall, leads to dysregulation of ACE 2, which in turn leads to a shift in the balance of RAAS towards activation of ACE 1 receptors, which have the opposite effects. ACE inhibitors and angiotensin receptor blockers (ARBs) play a key role in the treatment of major cardiovascular diseases such as hypertension and chronic heart failure, and today there is no evidence that ACE inhibitors or ARBs worsen severity of cardiovascular diseases. Therefore, it is not recommended to discontinue these drugs in patients with stable cardiovascular diseases and afflicted by COVID-19. The human recombinant hrACE 2 protein may be a potential therapy for CVI by blocking virus entry and eliminating the imbalance in RAAS.