ABSTRACT
Acute respiratory syndrome with various signs and outcomes caused by the SARSCoV-2 virus is the biggest challenge facing health systems worldwide today. The renin-angiotensin-aldosterone and kinin-kallikrein systems and within these two endopeptidases (ACE and ACE2) play a crucial role in the developing clinical feature of COVID-19. Adverse effects of the ACE-stimulated Ang II/AT1R axis (oxidant, pro-inflammatory effect, vasoconstriction) are counterbalanced by the ACE2-induced AT2R and MasR activities (antioxidant, anti-inflammatory effect, vasodilation). The severity of SARS-CoV-2 pneumonia and systemic inflammation explains the impairment of ACE2 (as an important defence factor of the lungs) caused by the biding spike protein of the SARS-CoV-2, which decreases the ACE2 levels. In parallel, bradykinin production also increases and intensifies the SARS-CoV-2-induced cytokine storm through the BKB1 and BKB2 receptors. Since the RAAS inhibitors (ACEI, ARB) affect the two regulatory systems and enzymes at different sites and to different degrees, their role must urgently have been clarified in the COVID-19 since their use is essential and general of many population-wide diseases (hypertension, cardiovascular, renal and metabolic conditions). Based on pathophysiological and experimental data, it is reasonable to hypothesize that in COVID-19 with comorbidities, especially in the elderly, the decreased ACE2 expression may be restored by RAAS inhibitors and the missed or reduced protective effect may be revitalised. This protective effect applies to both RAAS inhibitors. Clinical trials clearly support the declared opinion of many international societies that the use of RAAS inhibitors does not increase the risk of the occurrence of SARS-CoV-2 in itself let alone the severe and critical cases. Accordingly, initiated RAAS inhibitor therapy not only may rather must be continued during the development of COVID-19. © 2021 Literatura Medica Publishing House. All rights reserved.