My take on it is that so far we are talking about how people with high levels of ACE-2 receptors may be at higher risk of getting infected, but it does not explain why SARS-COV-2 migrates to system shutdown in some identified at risk groups.
It would indeed be a problem if the common 'pril meds actually increased the number of ACE-2 receptors, but there seems to be no evidence of that happening either way. The limited evidence so far only considers plasma born free ACE-2 so does not record the cell takeup as receptors, which is what the inhibitor aspect of a 'pril is about. So we do not know yet if a 'pril is a good guy or a bad guy, or just simply a goodbye in this worrisome time.