IJCS | Volume 33, Nº4, July and August 2020

408 Figure 2 – Schematic representation of the renin-angiotensin-aldosterone system in two different situations: in the absence and in the presence of pharmacological interventions using angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin II AT1 receptor blockers (ARBs). For each situation there is a highlighted axis (red) and a faded axis (blue). Angiotensinogen is produced in the liver as a renin (enzyme secreted by the kidney) substrate and generates angiotensin I (ANG I), an inactive peptide. Through the action of angiotensin-converting enzyme (ACE), ANG I is converted into angiotensin II (ANG II), which determines its effects by binding to its receptors AT1 (AT1R) and AT2 (AT2R). The action of angiotensin-converting enzyme 2 (ACE2) on ANG II leads to the production of angiotensin 1-7 (ANG 1-7), which determines various effects by binding to Mas receptors (MASR). Also, ACE2 is able to bind to S protein in the virion, favoring cell invasion by the new coronavirus. 13,14 of COVID-19 on the cardiovascular system may also involve reducing the availability of ACE2 in the heart. It was observed that the coronavirus increases myocardial inflammation, causing cardiac dysfunction possibly due to a decrease in the cardioprotective effects associated with the ACE2-Ang1-7-MasR axis. 17 Lippi et al., in their meta-analysis, demonstrated that cardiac Troponin I concentrations were significantly increased in patients infected with the new coronavirus, showing possible cardiac injury. 18 In turn, Guan et al., observed that 13.7% of 1099 patients with COVID-19 had increased Creatine-Kinase, and 37.2%, a high concentration of lactate dehydrogenase. 19 In addition, cardiac injury is further supported by a decrease in oxygen supply due to pulmonary insufficiency. 17 In view of this, it is worth discussing the use of drugs that negatively modulate the RAAS and can simultaneously increase the expression of ACE2 during the course of COVID-19. The expression / activity relationship of ACE2 regarding the use of ARB and ACEI is still unclear. However, studies in different experimental models (healthy rats, with acute Pedro et al. Cardiovascular pharmacotherapy and covid-19 Int J Cardiovasc Sci. 2020; 33(4):404-411 Viewpoint