Abstract :
Host cell penetration of SARS-COV-2 is mediated by angiotensin-converting enzyme 2 (ACE2), which is expressed on the
surface of epithelial cellslining the respiratory tract, cardiomyocytes, endothelial cells, and vascular smooth muscle cells (1).
Animal experiments have revealed that expression and activity
of ACE2 in various organs are increased with the administration
of angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs) (2). Therefore, previous speculations suggested worse outcomes in patients with COVID-19
with the use of renin–angiotensin system (RAS) inhibitors (3). Although, there is no evidence that shows an association of ACEIs
or ARBs with upregulation of ACE2 levels in human lung or cardiac tissues, higher urinary ACE2 levels documented in patients
with hypertension treated with ARBs suggest that upregulation
of ACE2 may also occur in humans (4, 5). These findings led to
the hypothesis that RAS inhibition by means of ACEIs and ARBs
may increase the risk of COVID-19 through upregulation of ACE2
and increase of viral load. ACE2 is a paralogue of ACE; however,
they have opposite effects (6). ACE2 downregulates the RAS
and acts as a deactivator of angiotensin II by converting it into
angiotensin-(1–7) which has opposite properties to angiotensin
II. Angiotensin II is an active peptide causing vasoconstriction,
fibrosis, and inflammation by binding to angiotensin 1 receptor
(AT1R). In contrast, angiotensin-(1–7) induces vasodilatation and
shows antifibrotic and anti-inflammatory properties (7).
