Interaction between RAAS inhibitors and ACE2 in the context of COVID-19
In the article, Interaction between RAAS inhibitors and ACE2 in the context of COVID-19, Jean-Jacques Mourad and Bernard Levy provides a medical research article based on the commentary of previous literature. The authors researched to determine the effects of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) to host cells through the ACE2 receptors, leading to the manifestation of coronavirus diseases (COVID-19)-based pneumonia. Mourad and colleague further comment that SArS-CoV-2 causes chronic damage and acute myocardial injury to the cardiovascular system.
The medical research scholars found that different renin-angiotensin-aldosterone system (RAAS) inhibitors present varying effects on angiotensin-converting enzyme 2 (ACE2) levels. The administration of ACE inhibitors or angiotensin-receptor blockers (ARBs) is essential in increasing the levels of Ace2 mRNA in rats. Mainly, the levels of Ace2 mRNA increase in rats provided an ARB or an ACE inhibitor. The researcher further established that losartan treatment, as opposed to lisinopril medication, increases the activity of ACE2 compared with placebo. Yet, the researchers failed to explain the mechanisms that tend to account for the reported differences. Treatment with an ACE inhibitor appears to significantly increase the expression of ACE2 protein in rats with acute lung injury.
The article reports that the protective effects of the ACE2-angiotensin promote primary mediation of the mas receptor axis based on the reduction in levels of angiotensin II. Therefore, RAAS inhibitors, including ARBs and ACE inhibitors, can activate the ACE2–angiotensin-(1–7)–Mas receptor axis. As the authors’ highlight, whether COVID-19 patients and hypertension that are taking an ARB or ACE inhibitor should use a substitute antihypertensive remains controversial. The researchers pinpoint a study that found the use of ACE inhibitor or ARB did not lead to increased levels of mortality in 112 patients with coronavirus and cardiovascular disorder. Additional evidence is needed to elucidate the impact of ARBs and ACE inhibitors in patients suffering from coronavirus diseases.
In March, the European Society of Hypertension published a report on the subject of hypertension, COVID-19, and RAAS blockers, deducing that the present data fails to support the differential application of ACE inhibitor and ARBs in patients with coronavirus. The authors went ahead to caution that the treatment associated with current evidence at the period of release and require necessary updates based on new evidence. The authors further clarified that different ACE inhibitors and ARBs have different effects on the levels of ACE-2. Particularly, RAAS inhibitors act at various levels to produce heterogeneous effects on the enzymes and peptides involved. Mineralocorticoid-receptor and angiotensin-receptor blockers have been found to increase ACE2 levels activity and expression in clinical and environmental models. However, the administration of ACE2 inhibitors augmented levels of cardiac Ace2 mRNA but does not have the effect of Ace 2 activity in experimental models.
In conclusion, Mourad and Levy’s research suggests that aliskiren treatment would also be a remarkable choice in the procedure for acute infection of respiratory syndrome coronavirus 2 (SARS-CoV-2). The authors suggest that aliskiren has the potential to reduce ACE2 expression. Even if ACE2 has been shown as the functional receptor for SARS-CoV-2, its role in connection to the progression of COVID-19 following infection with SARS-CoV-2 remains controversial. Hence the significance of aliskiren application patients with COVID-19 requires additional research. Patients with underlying SARS-CoV-2 and CVD disease present a severe prognosis. Consequently, there is a need to provide particular attention to the protection of cardiovascular in the process of COVID-19 treatment.