Commentary: Effect of Angiotensin-Converting-Enzyme Inhibitor and Angiotensin II Receptor Antagonist Treatment on ACE2 Expression and SARS-CoV-2 Replication in Primary Airway Epithelial Cells

Curbing activation of the renin-angiotensin-aldosterone system (RAAS) at various levels is considered the most effective protection in a number of cardiovascular pathologies. Two years of the Coronavirus disease 2019 (COVID-19) pandemic have revealed that therapeutic interference with the RAASmay be amuchmore complex issue than ever expected. During an acute stress reaction, the RAAS is the crucial neurohumoral actor covering high circulatory andmetabolic demands. On the other hand, long-lasting stimulation of the RAAS in the course of chronic cardiovascular disorders may result in undesirable target organ rebuilding and energy depletion, thus compromising cardiovascular health and life expectancy (Simko and Simko, 1999). The alternative angiotensin-converting enzyme (ACE)2/ angiotensin (Ang) 1–7/Mas receptor (MasR) pathway counterbalances the potentially harmful effects of the classical ACE/AngII/angiotensin II type 1 receptor (AT1R) pathway; hence, well balanced cooperation between these two pathways preserves the prevalence of benefits over the potential harm (Steckelings and Sumners, 2020; Simko et al., 2021).