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Angiotensin Ii


jangle
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http://www.ncbi.nlm....v/pubmed/512963

I found this study that showed that angiotensin ii concentration effectively blocks nerve signals from the vagus nerve. Essentially what I think is happening is that systemically (kidneys, brain, heart) there is an elevated level of angiotensin ii (Might show up in serum samples, might not - for those that it doesn't, the angiotensin ii might only be localized to certain regions - perhaps due to localized ACE2 autoantibodies.)

I don't think it is the nerve that is damaged but rather the method for the nerve to communicate its signals to the various organs.

Interestingly enough I think this might also have a role in anxiety disorders. People with mitral valve prolapse often have anxiety/dysautonomia and sure enough this study showed they have a faulty angiotensin ii system: http://www.ahjonline...0015-9/abstract

Now that's more of a speculation.

Anyways, I recently got referred to Doctor Levine and I sent him my idea about angiotensin ii/vagus nerve. He said he was very impressed and that he will have a lot to talk about with me. I know of all the POTS researchers he's the most steadfast against there being a problem with the autonomic nervous system. But I have found that life is full of ironies.

EDIT: Also, I think the reason Astronauts develop POTS is because their angiotensin ii levels go up during spaceflight.

http://www.ncbi.nlm.nih.gov/pubmed/2147850

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Good thoughts jangle. I had my ang 2 tested on Friday so I will let you know when I get the result. If anyone on here should have elevated ang 2 based on your theory it would be me due to my autoimmune history and hyper pots presentation. About the astronauts though- I read research that they have proven that their OI is caused by nitric oxide problems, not ang2. Just a thought.

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Julie that is true. A higher angiotensin ii level shouldered make a high aldesterone level. There has to be something going on one abstraction level above what we are looking at. I don't think it is a dysfunction of the receptors because that would cause chronic symptoms i.e. structurally abnormal nerve receptors would have produced POTS all of one's life, but because POTS is something that one develops it suggests an alteration in chemical environment rather than structural genetic change. However I do think it is possible to have elevated angiotensin ii in localized regions I.e. the heart perhaps has a local deficiency of ace ii enzymes while maintaining overall serum levels constant.

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That makes sense Jangle. I read an article about research on mice where they were able to make them have high ang2 without elevated BP by manipulating a gene expression. They said the rats only had elevated ang2 in the endothelium.

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http://www.heartrhyt...1204-X/abstract

Julie, also I found in this article that despite POTS patients having higher angiotensin ii levels, they had similar to slightly lower aldesterone numbers. (p = .111) only p < 0.05 is considered statistically significant. So in other words there was not a statistically significant difference in aldesterone levels between POTS and controls.

Now why that is? I have no idea.

EDIT: Lemons I would love for Rama to help me mow my lawn.

Did that sound as wrong as it did to me?

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Gees - interesting stuff there mate. Awesome finds regarding ang II and mitral valve prolapse syndrome. I had no idea about that. I think ang II obviously plays a big role - or is the primary pathophysiology in those with elevations. Just need to start getting these doctors to check it!

Dr Levine is more open to alternative ideas than some of the research suggests.I hear murmurs that there is acknowledgement that exercise only permanently cures a minority. He is very interested in the blood volume angle according to a patient of his.

Space flight is weird - it either messes with ang II or it messes with Nitric oxide, both being implicated increasingly in POTS.

Vagus nerve is also an interesting angle. I often wonder whether the over stim from POTS is caused by vagal withdrawal as it also occurs in all postural disorders so it cant be ( i dont think) beta hypersensitivity). But if ang II blocks the vagus Im condused about what that would do. Could ang II actually help those POTSies without elevated ang II by blocking the vagus? I think what often happens in POTS is there is parasympathetic withdrawal. this is in response to reduced sroke volume. But the consequences of this withdrawal are interesting.

On the on hand Dr S thinks that ang II results in increased sympathetic activity, reduced NO and potentiated NE with vasomotor failure. Vanderbilt think that increaased ANG II results in reduced ang II receptor activity and impaired ang II vasoconstriction in the stomach area. I like the later just because its simpler. I guess we are getting somewhere here at least.

Ill get the lawnmower primed and ready for the 12 hour flight (Melb Aus to ???, US).

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Ya Rama, I'm beginning to think that the therapeutic value of Florinef isn't just an enhancement of blood volume, but rather I think it is doing an activity similar to spironolactone. Dr. Stewart did mention that Florinef is essentially artifical spironolactone, and if spironolactone drastically raises ACE2 levels and lowers angiotensin ii, then maybe Florinef is having some type of attenuated ACE2 enhancement as well. Still, I think spironolactone would have a much more drastic ACE2 elevation effect.

Either way, there might be an even better therapeutic option for raising ACE2 levels/lowering angiotensin ii. Exercise might work for some, but I got to believe there's some type of hormonal medication that would also work well. I've been searching but thusfar I haven't found anything outside of the herbs and spironolactone already posted.

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Ya Rama, I'm beginning to think that the therapeutic value of Florinef isn't just an enhancement of blood volume, but rather I think it is doing an activity similar to spironolactone. Dr. Stewart did mention that Florinef is essentially artifical spironolactone, and if spironolactone drastically raises ACE2 levels and lowers angiotensin ii, then maybe Florinef is having some type of attenuated ACE2 enhancement as well. Still, I think spironolactone would have a much more drastic ACE2 elevation effect.

Either way, there might be an even better therapeutic option for raising ACE2 levels/lowering angiotensin ii. Exercise might work for some, but I got to believe there's some type of hormonal medication that would also work well. I've been searching but thusfar I haven't found anything outside of the herbs and spironolactone already posted.

Now your thinking! LKicorice root also has effects on ang II and ace2.

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Either way, there might be an even better therapeutic option for raising ACE2 levels/lowering angiotensin ii. Exercise might work for some, but I got to believe there's some type of hormonal medication that would also work well. I've been searching but thusfar I haven't found anything outside of the herbs and spironolactone already posted.

Well, what about ARBs like Losartan? My son has been on it for a year with no side effects (that we're aware of). He certainly sees benefit from it!

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Either way, there might be an even better therapeutic option for raising ACE2 levels/lowering angiotensin ii. Exercise might work for some, but I got to believe there's some type of hormonal medication that would also work well. I've been searching but thusfar I haven't found anything outside of the herbs and spironolactone already posted.

Well, what about ARBs like Losartan? My son has been on it for a year with no side effects (that we're aware of). He certainly sees benefit from it!

The info I found on the autoantibodies to ACE2 said that IF this is the problem an ARB shouldn't be used because it affects the baroreflex but an ACE would be the way to go. The ARB will increase potassium levels and IF this is the problem - then there are issues with increased potassium. So, maybe an ACE if there are autoantibodies to ACE2? That's all I came across if this is the problem.

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Angiotensin II itself effects baroreflex sensitivity. An ARB would block the effects of angiotensin II, reducing baroreflex abnormalities, reducing oxidisive stress and improve downregulation of ang II cardiovascular receptors. It is also quite possible that autoantibodies are activating or 'clogging up' ang II receptors forcing the body to reduce ace 2 and increase Ang II to compensate. if this were the case (and the early research evidence seems to suggest otherwise perhaps) then sure an ARB might not be best, but an ACE inhibitor wouldnt help either.

ACE inhibitors suppress all angiotensins, reduce stroke volume and cardiac output. if there was faulty ace 2 youd be far better off just trying to normalise ang II than messing with all angiotensins I would presume.

The fact that POTSies with high Ang II responded less to an additional ang II infusion suggests that the levels are high and the receptors are downregulated. So reducing sensitivity of those receptors by blocking ang II reception should cause upregulation - in theory...

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honestly the best way to go would be just to get some synthetic ace2 enzymes and throw em in. Don't know if that's possible. If we can get a researcher interested, they might have some ideas.

Never heard of one before and I'm pretty up on natural supplements. It would have to be something newly discovered.

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Angiotensin II itself effects baroreflex sensitivity. An ARB would block the effects of angiotensin II, reducing baroreflex abnormalities, reducing oxidisive stress and improve downregulation of ang II cardiovascular receptors. It is also quite possible that autoantibodies are activating or 'clogging up' ang II receptors forcing the body to reduce ace 2 and increase Ang II to compensate. if this were the case (and the early research evidence seems to suggest otherwise perhaps) then sure an ARB might not be best, but an ACE inhibitor wouldnt help either.

ACE inhibitors suppress all angiotensins, reduce stroke volume and cardiac output. if there was faulty ace 2 youd be far better off just trying to normalise ang II than messing with all angiotensins I would presume.

The fact that POTSies with high Ang II responded less to an additional ang II infusion suggests that the levels are high and the receptors are downregulated. So reducing sensitivity of those receptors by blocking ang II reception should cause upregulation - in theory...

Okay, so where's my brown rice? Rama, any other ideas to do this other than an ARB or ACE?

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