ACE and ACE2 are different proteins. The ACE protein, the drug target for ACE inhibitors, converts Angiotensin I to Angiotensin II, which then is bound to the AT1R receptor (blocked by the ARB drugs) causing, indirectly, vasoconstriction and elevation of blood pressure.
ACE2 is a counter-regulatory protein to ACE. It binds Angiotensin II and converts it to Ang(1-7). Ang(1-7) eventually binds to the mas receptor and causes vasodilation and lowering of BP. There has been a fair amount of speculation about the potential that mas could be a drug target, but I’ve not heard of anything close to the clinic yet.
ACE2 is not affected by classical ACE inhibitors.
The binding site of 2019-nCoV is distinct from the active site of the enzyme. Binding results in endocytosis of the virus particle. The ACE2 protein is not known otherwise to function as a receptor; that is, there’s no known endobiotic substance that internalizes upon binding to ACE2, but both the SARS and 2019-nCoV viruses express a xenobiotic protein that has the effect.
Binding of 2019-nCoV to the ACE2 site may account for the increased death rate among hypertensive COVID-19 patients, if it interferes with the AngII->Ang(1,7) pathway. That would make ARB’s or ACE inhibitors protective against some of the disease’s effects by blocking the effects of the unconverted AngII, without interfering with the virus’s infectious pathway.
