ACE Inhibitors - why work to increase plasma renin?

[UhHuh 714]

I'm a new student and I came across something that is driving me crazy if someone can please answer and help!

Reading on ACE Inhibitors describes how they work, which I understand how they work on Ang II, however, the drug guide book also states, "ACE inhibitors also ↑ plasma renin levels and ↓ aldosterone levels. Net result is systemic vasodilation." Why would an antihypertensive therapeutically work to INCREASE renin? I suppose negative feedback would result in ↑ plasma renin, but the drug guides state this as a therapeutic action. I can't understand this for the life of me. Please someone, help!

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[aboveliquidice]

I'm a new student and I came across something that is driving me crazy if someone can please answer and help!

Reading on ACE Inhibitors describes how they work, which I understand how they work on Ang II, however, the drug guide book also states, "ACE inhibitors also ↑ plasma renin levels and ↓ aldosterone levels. Net result is systemic vasodilation." Why would an antihypertensive therapeutically work to INCREASE renin? I suppose negative feedback would result in ↑ plasma renin, but the drug guides state this as a therapeutic action. I can't understand this for the life of me. Please someone, help!

Look at the MOA specifically... How do ACE-Is exert their action on the RAAS???

 

[pharm B]

Thread now open for business.

 

[owlegrad]

Thread now open for business.

Good Call!

 

[crazybob]

I'm a new student and I came across something that is driving me crazy if someone can please answer and help!

Reading on ACE Inhibitors describes how they work, which I understand how they work on Ang II, however, the drug guide book also states, "ACE inhibitors also ↑ plasma renin levels and ↓ aldosterone levels. Net result is systemic vasodilation." Why would an antihypertensive therapeutically work to INCREASE renin? I suppose negative feedback would result in ↑ plasma renin, but the drug guides state this as a therapeutic action. I can't understand this for the life of me. Please someone, help!

Although converting enzyme inhibitors are most effective in conditions associated with high plasma renin activity, there is no good correlation among subjects between plasma renin activity and antihypertensive response. Accordingly, renin profiling is unnecessary."

hope that helps.

 

[UhHuh 714]

Ok, I think I'm seeing the light now. Thanks for your posts. I have read that HTN associated with increased renin responds favorably with ACE inhibitor therapy. So I guess I can then see why ACE inhibitors would want to increase renin levels. I'll try to leave it at that. Just got so confused because renin is what starts the whole RAAS process to increase bp.

 

[mickfan13]

Ok, I think I'm seeing the light now. Thanks for your posts. I have read that HTN associated with increased renin responds favorably with ACE inhibitor therapy. So I guess I can then see why ACE inhibitors would want to increase renin levels. I'll try to leave it at that. Just got so confused because renin is what starts the whole RAAS process to increase bp.

not quite

increased renin is not a therapeutic mechanism of ace inhibitors, but it does happen due to negative feedback

it's simply inconsequential if high renin results from the negative feedback loop, because the angiotensin I that gets formed has no chance of getting converted to angiotensin II due to the presence of the inhibitor

 

[HaloKing]

not quite

increased renin is not a therapeutic mechanism of ace inhibitors, but it does happen due to negative feedback

it's simply inconsequential if high renin results from the negative feedback loop, because the angiotensin I that gets formed has no chance of getting converted to angiotensin II due to the presence of the inhibitor

my new word of the week.. thanks!

 

[aboveliquidice]

not quite

increased renin is not a therapeutic mechanism of ace inhibitors, but it does happen due to negative feedback

it's simply inconsequential if high renin results from the negative feedback loop, because the angiotensin I that gets formed has no chance of getting converted to angiotensin II due to the presence of the inhibitor

Ding!

 

[IrishHammer]

not quite

increased renin is not a therapeutic mechanism of ace inhibitors, but it does happen due to negative feedback

it's simply inconsequential if high renin results from the negative feedback loop, because the angiotensin I that gets formed has no chance of getting converted to angiotensin II due to the presence of the inhibitor

Juxtaglomerular apparatus FTW.

 

[Farcus]

If I remember right, its because lost of negative feedback. I forgot the exact mechanism but I'm quite sure it is lost of negative inhibition. Furthermore, the increase in Renin actually will increase production of other compounds since now there is a increase deposit and the Le Chatlier principle of high to low. That was like one reason why ACE-I isn't as good as ARB i think, although ACE-I is generally used more than ARB because there is more clinical date from its use than ARB. I could be totally wrong lol.

 

[b1234]

I would guess a there are two main reasons why ACE inhibitors are used more than ARB's.

ACE inhibitors have been around a lot longer so there are many people that have been on them for a very long time (before ARB's were available) - and they're working - so they continue on them. Also many prescribers originally learned ACE to prescribe ACE inhibitors and got in the habit of prescribing them - before ARB's were available so they tend to think of ACE inhibitors before they think of ARB's.

ARB's (even generics) are still considerably more expensive than ACE inhibitors also.

 

[quartel]

not quite

increased renin is not a therapeutic mechanism of ace inhibitors, but it does happen due to negative feedback

it's simply inconsequential if high renin results from the negative feedback loop, because the angiotensin I that gets formed has no chance of getting converted to angiotensin II due to the presence of the inhibitor

titcr.

I gotta admit, the original wording the OP wrote down confused me.