The SARS-Covid 19 pandemic has hailed the spotlight on a relatively new component of the renin-angiotensin-aldosterone axis called ACE2, angiotensin converting enzyme 2. When scientists elaborated the pathophysiology of SARS-Covid 19, they discovered the viral receptor was ACE2. ACE2 is expressed on the apical surface of respiratory epithelial cells. This is initiated a plethora of studies that investigated the link between SARS-Covid19 and the renin-angiotensin-aldosterone-axis. ACE2 is not only the viral receptor for SARS-CoV-2, but it’s an important antagonist in the renin-angiotensin-aldosterone-axis. The renin-angiotensin-aldosterone axis is an important component of the cardiovascular system. It has been extensively studied for over a century in order to elucidate the physiological and therapeutic facets. Along with this study another arm of the RAS has been discovered, which is believed to bring about a counter-regulatory effect. The metabolic end-products of angiotensin I and angiotensin II are key players in cardiovascular physiology and pathophysiology. This non-canonical axis consists of angiotensin 1-7, angiotensin 1-9, angiotensin converting enzyme 2, the type 2 angiotensin II receptor (AT2R), the proto-oncogene Mas receptor and the Mas-related G-protein coupled receptor member D. Each of these component has been shown to counter-regulate the effects of the classical angiotensin system. This counter-regulatory renin-angiotensin system has a central role in the pathogenesis and development of various cardiovascular diseases. Indeed many animal studies have elaborated the cardio-protective effects of the components of the counter-regulatory RAS. Therefore they represent a potential therapeutic target in the management of cardiovascular disease. In this thesis we will demonstrate ACE2 in particular and elucidate how it is a potential target for the therapy of cardiovascular disease.