[snapetom]

So, looking at the NIH conclusion, if I'm on a *saratan and read this:

"Selective blockade of either Ang II synthesis or activity induced increases in cardiac ACE2 gene expression and cardiac ACE2 activity, whereas the combination of losartan and lisinopril was associated with elevated cardiac ACE2 activity"

should I check in with my cardiologist?

[rolph]

first off drugs that influence the components of the RAS are not childs play, so yes consult your doctor[s] rather than experimenting with dosages.

This is only just starting to see clinical trials, meaning the people involved are under direct physician supervision.

regarding ACE2:

this increased production of ACE2 is an indirect effect of ACE2 disruption.

you have to be careful with these sorts of experiments. when you block angiotensin II receptors that means there is a reduction of signal for angiotensin II being present.

This angiotensin that would ordinarily be interacting with the ATreceptors is now available for ACE2 to operate upon.

the summary here is that increased enzymatic product doesnt mean the enzyme has been "turbocharged" . If there is an increased ratio of reactants to products this will cause increased concentration of products in total but does not change the intrinsic rate at which the enzyme actually operates.

This looks like a case of substrate concentration dependent equilibrium driving reaction rate.

[snapetom]

Thank you very much for the info and taking a look at it!

[rolph]

basically ACE2 is a regulator that converts between angiotensin II <--> angiotensin 1,7

these have opposite effects , angiotensin II is a vaso-constrictor, thus increases blood pressure.

angoitensin 1,7 is a vaso-dialator, thus decreases blood pressure. so there is an equilibrium state of the two established by ACE2. this is something that ACE inhibitors or ARB blockers dont directly influence.