Angiotensin-converting enzyme 2 (ACE2), a component of the renin-angiotensin system, is a receptor for SARS-CoV-2, the virus that causes
COVID-19. To determine whether the
renin-
angiotensin inhibition regulates ACE2 expression, either
enalapril (an
angiotensin-converting enzyme inhibitor) or
losartan (an AT1 receptor blocker) was infused subcutaneously to male C57BL/6J mice for two weeks. Neither
enalapril nor
losartan changed abundance of ACE2
mRNA in lung, ileum, kidney, and heart. Viral entry also depends on transmembrane
protease serine 2 (TMPRSS2) to prime the S
protein. TMPRSS2
mRNA was abundant in lungs and ileum, modest in kidney, but barely detectable in heart. TMPRSS2
mRNA abundance was not altered by either
enalapril or
losartan in any of the 4 tissues. Next, we determined whether depletion of
angiotensinogen (AGT), the unique substrate of the renin-angiotensin system, changes ACE2 and TMPRSS2
mRNA abundance. AGT
antisense oligonucleotides (ASO) were injected subcutaneously to male C57BL/6J mice for 3 weeks. Abundance of ACE2
mRNA was unchanged in any of the 4 tissues, but TMPRSS2
mRNA was significantly decreased in lungs. Our data support that the
renin-
angiotensin inhibition does not regulate ACE2 and hence are not likely to increase risk for
COVID-19.