COVID-19 (Coronavirus Disease 2019) is a pandemic infection caused by the Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2). Once in the body, COVID-19 can cause acute respiratory distress syndrome (ARDS) and multiorgan failure. The mandatory cellular structure for virus invasion is the membrane-bound form of angiotensin-converting enzyme 2 (ACE2). After SARS-CoV-2/ACE2 binding, this complex is internalized by the host cell, RNA is released and viral replication starts. ACE2 is part of the renin-angiotensin-system (RAS), that is critical in the physiological regulation of several body systems and specially in cardiovascular and blood pressure maintenance. The primary role of the positive RAS axis, by the ACE1 isoform, is to increase sympathetic nervous system tension, cause vasoconstriction, increase blood pressure, and promote inflammation, fibrosis, and myocardial hypertrophy. On the other hand, ACE2 acts in an opposite way to counteract these actions and maintain homeostasis. It is well established that RAS axis is directly related to the changes observed in hypertension pathophysiology. Thus, this work proposes to analyze the role of ACE2 in hypertension as a risk factor for COVID-19 and to evaluate the related emerging therapeutic strategies.