Benicar blocks the RECEPTORS (on cells) that allow Angiotensin II to be used by the body. It actually induces INCREASED production of the hormone itself (angiotensin II) as your body tries to adjust for the lack of availability of the hormone at its receptors. You will find that serum ACE also rises while an Angiotensin Receptor Blockade is in place.
ACE (angiotensin converting enzyme) is an intermediate biochemical. It is a precursor to Angiotensin. It has no direct action in the inflammatory cycle other than to cause the release of quantities of Angiotensin II. That is probably why it is relatively insignificant in some patients; it depends on your Renin Angiotensin System activity level.
The more your ACE is initially elevated, the more ACE is being generated in your inflammation, and the higher the ACE will go when the Angiotensin II receptors are blocked. We have had one report of ACE greater than 400.
The serum ACE usually rises to quite high levels when you have an Angiotensin Receptor Blockade in place (eg with Benicar).
This is because the inflamed tissue can't get any Angiotensin II binding at its receptors, so it puts out extra ACE to try and convert more Renin/A-1 into Angiotensin II (the Angiotensin-II level rises too). But even though all that Angiotensin II is manufactured, there are no receptors left for it to bind to, so it can do no harm.
Note that ACE is not the same as Angiotensin II. They are different chemicals and have vastly different functions. Our paper "New Treatments Emerge..." describes the biochemistry at "the Angiotensin Hypothesis". Although put as a 'hypothesis' in that (old) paper, a Spanish group recently validated my etiology in-vitro and in rats.
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