jangle Posted February 7, 2012 Report Share Posted February 7, 2012 http://www.ncbi.nlm....v/pubmed/512963I 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/abstractNow 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 Quote Link to comment Share on other sites More sharing options...
julieph85 Posted February 7, 2012 Report Share Posted February 7, 2012 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. Quote Link to comment Share on other sites More sharing options...
jangle Posted February 7, 2012 Author Report Share Posted February 7, 2012 Julie I've heard the method of testing angiotensin ii is quite involved so hopefully they did it right. There could be a connection between nitric oxide and angiotensin ii. Quote Link to comment Share on other sites More sharing options...
julieph85 Posted February 7, 2012 Report Share Posted February 7, 2012 All I know is you have to be fasting, it should be taken in the supine position, and a special chemical gets added to the vial. That's all I know and that's what they did. Hopefully it will be accurate Quote Link to comment Share on other sites More sharing options...
julieph85 Posted February 7, 2012 Report Share Posted February 7, 2012 Something I have thought about though- if your ang 2 is high so should your aldosterone. I've had mine checked and it is normal. Quote Link to comment Share on other sites More sharing options...
jangle Posted February 7, 2012 Author Report Share Posted February 7, 2012 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. Quote Link to comment Share on other sites More sharing options...
Maiysa Posted February 7, 2012 Report Share Posted February 7, 2012 Thanks for the information Jangle. Wonderful research. So glad Dr. Levine is open to your thoughts. Good work! Quote Link to comment Share on other sites More sharing options...
julieph85 Posted February 7, 2012 Report Share Posted February 7, 2012 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. Quote Link to comment Share on other sites More sharing options...
Lemons2lemonade Posted February 7, 2012 Report Share Posted February 7, 2012 Jangle, sounds like rama may be doing some yard work over at your place soon keep up the good work! Quote Link to comment Share on other sites More sharing options...
jangle Posted February 7, 2012 Author Report Share Posted February 7, 2012 http://www.heartrhyt...1204-X/abstractJulie, 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? Quote Link to comment Share on other sites More sharing options...
ramakentesh Posted February 7, 2012 Report Share Posted February 7, 2012 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). Quote Link to comment Share on other sites More sharing options...
ramakentesh Posted February 7, 2012 Report Share Posted February 7, 2012 Wrong? me mowing lawns? Im pretty good at it actually...Yeah high ang II = low ald and renin in pots for unknown reasons. Quote Link to comment Share on other sites More sharing options...
jangle Posted February 7, 2012 Author Report Share Posted February 7, 2012 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. Quote Link to comment Share on other sites More sharing options...
ramakentesh Posted February 7, 2012 Report Share Posted February 7, 2012 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. Quote Link to comment Share on other sites More sharing options...
Lenna Posted February 8, 2012 Report Share Posted February 8, 2012 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! Quote Link to comment Share on other sites More sharing options...
ramakentesh Posted February 8, 2012 Report Share Posted February 8, 2012 Lenna - that would ofcourse be better.Any specific symptoms that your son experienced that might make him stand out from the average potsie? Cold all the time? pooling? bad reaction to beta blockers? etc. Quote Link to comment Share on other sites More sharing options...
issie Posted February 8, 2012 Report Share Posted February 8, 2012 All I know is you have to be fasting, it should be taken in the supine position, and a special chemical gets added to the vial. That's all I know and that's what they did. Hopefully it will be accurate Who did your test for you? Quote Link to comment Share on other sites More sharing options...
issie Posted February 8, 2012 Report Share Posted February 8, 2012 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. Quote Link to comment Share on other sites More sharing options...
jangle Posted February 8, 2012 Author Report Share Posted February 8, 2012 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. Quote Link to comment Share on other sites More sharing options...
ramakentesh Posted February 8, 2012 Report Share Posted February 8, 2012 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... Quote Link to comment Share on other sites More sharing options...
ramakentesh Posted February 8, 2012 Report Share Posted February 8, 2012 I think both Vanderbilt and Stewart/Medows are very interested in this area, although estimates of the amount of POTS patients that this relates to varies from 20%-25% upwards. Quote Link to comment Share on other sites More sharing options...
issie Posted February 8, 2012 Report Share Posted February 8, 2012 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. Quote Link to comment Share on other sites More sharing options...
issie Posted February 8, 2012 Report Share Posted February 8, 2012 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? Quote Link to comment Share on other sites More sharing options...
ramakentesh Posted February 8, 2012 Report Share Posted February 8, 2012 Im looking Salvia elegens?? Quote Link to comment Share on other sites More sharing options...
jangle Posted February 8, 2012 Author Report Share Posted February 8, 2012 http://www.ncbi.nlm....pubmed/20228119Could this explain why saline helps POTS patients but not water + salt intake? (not as much anyway) It seems angiotensin ii affects something about water intake, but not saline intake. Quote Link to comment Share on other sites More sharing options...
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