RAAS
renin–angiotensin–aldosterone System
ACE2 is a widely expressed protein, and it plays a major regulatory role in the renin–angiotensin–aldosterone System (RAAS).
We additionally explored the hypothesis that SARS-CoV-2 favors the internalization of membrane ACE2 receptors generating an imbalance of the renin-angiotensin-aldosterone system (RAAS), increasing the activity of angiotensin II (ANG-II), disintegrin, and metalloproteinase 17 domain (ADAM17/TACE), eventually modulating the integration of afferents reaching the NTS from baroreceptors and promoting increased blood pressure.
The problem of studying the association between AH and COVID-19 is also very relevant from an etiopathogenetic point of view, since, both in the development of COVID-19 and in the pathogenesis of AH, one of the key places is occupied by the components of the renin-angiotensin-aldosterone system (RAAS) and, first of all, turn, angiotensin-converting enzyme-2 (ACE-2) and angiotensin II (AII).
Background : Angiotensin-converting enzyme inhibitors (ACEi) and angiotensin-II receptor blockers (ARB), the most commonly prescribed antihypertensive medications, counter renin-angiotensin-aldosterone system (RAAS) activation via induction of angiotensin-converting enzyme 2 (ACE2) expression.
Abstract Context The SARS-CoV2 virus is dependent on components of the renin-angiotensin-aldosterone system (RAAS) for infectivity.
One of the essential regulators of arterial blood pressure, the renin-angiotensin-aldosterone system (RAAS) seems to be one of the most complex mechanisms in the human body.