Influence of SARS-CoV-2 Infection on the Renin Angiotensin System

ABSTRACT

The advent of coronavirus-2019 (COVID-19) as a global pandemic has prompted scientists to address an urgent need to clarify the disease's pathogenic mechanisms and treatment. Severe acute respiratory syndrome is the severe complication of coronavirus 2 (SARS-CoV-2). This novel coronavirus uses the angiotensin 2 converting enzyme (ACE2) as a key target for cell surface attachment as well as a possible entry point into the host cell. Thus, for clinical intervention, a correct understanding of the elements that can influence the expression and function of ACE2 in the healthy and diseased body is critical. Over 60% of all persons in Europe have comorbidities, necessitating the usage of a prescription drug. While prior research has focused on the use of reninangiotensin inhibitors (RAS) to regulate ACE2 expression, new evidence in the literature suggests that a number of commonly used medicines for hypertension, heart failure, diabetes, and hyperlipidemia may interfere with COVID-19 infection. The involvement of the renin-angiotensinaldosterone system in the pathology of various complications such as hypertension and chronic kidney disease, through its aldosterone-releasing effects, stimulates coronary vasoconstriction, especially in the already ischemic heart. We offer a brief discussion of the methods through which medications that interfere with the renin-angiotensin system may influence the viral entrance of SARS-CoV-2 into cells, in addition to their known therapeutic effects.