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Jangle - I'm Trying To Understand What You Are Saying - Help Clarify


futurehope
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Jangle,

You spoke to a doctor about ACE2? What exactly did you speak to the doctor about, and what is ACE2 and what does it have to do with POTS?

I'm not on this forum much anymore, so I've missed your drift.

Thanks in advance.

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ACE2 is an enzyme that converts angiotensin2 to angiotensin (1-7). If one lacks ACE2, then higher levels of angiotensin2 will build up. Angiotensin2 is found all over the body and it is a relatively new protein that has been identified. Recent studies have implicated Angiotensin2 in heart function, inflammation, and even autonomic function.

Dr. Stewart was the first researcher to identify that POTS patients seemed to have higher levels of angiotensin2 in their bodies. Additionally, Dr. Raj at Vanderbilt replicated this finding. It is thought that some POTS patients have lower levels of ACE2 enzyme. In 2010 it was found that there are autoantibodies that attack ACE2 enzyme. It's not known currently if POTS patients have this autoantibody. There could also be genetic factors that explain why POTS patients have higher angiotensin2 levels.

I spoke with Dr. Stewart about potentially using Spironolactone to treat this ACE2 deficiency, he said that it might have an adverse effect in some patients because spironolactone is a diuretic, but that it is a thought.

Additionally, he said that other studies have shown that aerobic exercise has balanced the ACE2 levels in animal models.

Vitamin D has also been inversely correlated with angiotensin2 levels. Low vitamin D levels seem to produce high angiotensin2 levels. Therefore, correcting a vitamin D deficiency might also be therapeutic.

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It sounds good, but I have a thought. I'm not trying to be negative, but to understand. If hyperPOTS patients have higher angiotensin II due to faulty production of ACE2, then that would cause higher b/p, right? If this is true, then that should be true across the board, whether we are standing, sitting or lying down, right? I'm not sure about others, but my b/p is very normal sitting, like 115/78, but on the TTT goes to 170/110. We can't have a "selective" lack of ACE2, as in only when standing. I am trying to figure this out, so please correct me if I don't understand the whole concept, because I am game for finding the answer! And, it could be VERY likely that my brain is just plain not understanding all this! :)

So, help me understand how the theory from the research centers explains normal b/p when not standing.

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It sounds good, but I have a thought. I'm not trying to be negative, but to understand. If hyperPOTS patients have higher angiotensin II due to faulty production of ACE2, then that would cause higher b/p, right? If this is true, then that should be true across the board, whether we are standing, sitting or lying down, right? I'm not sure about others, but my b/p is very normal sitting, like 115/78, but on the TTT goes to 170/110. We can't have a "selective" lack of ACE2, as in only when standing. I am trying to figure this out, so please correct me if I don't understand the whole concept, because I am game for finding the answer! And, it could be VERY likely that my brain is just plain not understanding all this! :)

So, help me understand how the theory from the research centers explains normal b/p when not standing.

Sue, I agree and was thinking the same thing myself.

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I don't know the answer and I can't speak to the specific population of hyperpots. However, I do know that ACE2 is found inside neurons in the regions of the brain that coordinate and control autonomic activity. It is unlikely that angiotensin2 is the sole cause of POTS, because there are many other patient populations with higher levels of angiotensin2 that do not have autonomic dysfunction.

However, that does not mean that angiotensin2 does not have a role, it may be a faulty compensatory mechanism, or serve as an aggravating factor of POTS.

Blood pressure is controlled by many different physiological mechanisms. Perhaps in a supine position or sitting position, the other compensatory mechanisms are sufficient to control blood pressure. But upon standing up, the stress is sufficient to break through the compensatory mechanisms and cause the typical oscillating or elevated blood pressure exhibited in POTS.

Alternatively your autonomic system could be partitioned.

That is to say, that when you are sitting down, one part of your autonomic system controls your blood pressure and hemodynamics, and when you stand up, the brain registers the process of standing up and switches to another system or part of your body to control the hemodynamics there. In the process, if someone had a faulty mechanism on this side, it would produce the OI. Perhaps the elevated ACE2 concentrations are in the parts of the brain that originally are supposed to control hemodynamics in a standing position only.

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Jangle,

I have taken Spironolactone in the past, a very low dose (25 mg/day), to combat hair loss (believe it or not). Is ingestion of Spironolactone supposed to decrease angiotensin II levels? You've got me more curious than ever because the taking of Spironolactone was against my neurologist's wishes. He was convinced it would make my POTS worse.

In any event, until I get angiotensin II levels measured, I have no idea if I am circulating higher levels or not?

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I don't know for sure if my son has high angiotensin II or not...he was never tested. However, he was tested for nitric oxide levels (as part of a clinical study) and we know that his NO levels were deficient (which would lead me to conclude that his angiotensin is high). He was put on Losartan - an angiotensin II receptor blocker - and he went from being profoundly disabled to mildly disabled over the past 9 months. Which again, leads me to conclude that his angiotensin II was high. However, he has never had blood pressure issues. Not sitting, not standing. With the Losartan, his blood pressure started getting a little low, so he is now taking Florinef to compensate for that and it seems to have evened out his BP for the most part.

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Woa, I really want to back up for a second here and make this statement.

I absolutely do not advocate anyone using spironolactone based off of what I have said. I am just a random internet user, with no professional medical education. The guy with professional medical education and experience with POTS has said that spironolactone might have an adverse effect in patients. I really don't want anyone to take this on my behalf and have it hurt them. In my own personal case, I'd be willing to experiment with it simply because that is a personal decision made by me based on absolutely no safety research or plausibility of effects outside of abstract ACE2 levels.

That being said,

futurehope, how did spironolactone work for you? Also yes, spironolactone would very much decrease angiotensin2 levels. It increases the ACE2 enzyme by as much as 3 times. But please refer to the statement I made above about using Spironolactone for POTS.

Lenna that is very interesting. I'll have to look into Losartan more.

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Jangle,

I'm sorry I scared you into thinking I would use something you suggested. I have been asking all my questions because I already have a prescription for 25 mg Spironolactone, and I have been taking it for over a year.

Like I said previously, when my POTS doctor heard about me taking Spironolactone (for hair loss), he said "Why?" "That is going to make you worse?" I ignored him and took it any way. (That's what being vain will do for ya!)

Anyhow, to answer your question, I don't really know one way or another if the 25 mg Spironolactone helped or hurt my POTS. But I can say that I survived over a year taking it, and that year included me going to a fitness center.

So, that's why I'm asking all the questions. I would not do or take anything based on your suppositions. But, you can understand my curiosity in light of the fact that I had already been taking Spironolactone.

Keep up the good internet researching. I appreciate it.

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There is a test for ang II done by Quest Diagnostics

Why doesnt angi II result in hypertension? Good question - low blood volume? reduced stroke volume? low vasomotor blood flow? The studies all indicate this.

In the vandy study the patients had high ang II but low ang ii mediated vasoconstriction. So sympathetic excess was to compensate for this.

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Well, now that's something we can do--test our ang. II levels! If my doctor doesn't test it next week, I can test it when I get back. If a few others are up for it, we'll see if there's a trend.

Did I die and go to heaven??!! I'm just loving all this "research" on the forum lately!

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FWIW I have orthostatic hypOtension, and aerobics led to my eventual POTS dx. I can't go more than 5 minutes into an aerobic workout before all the positional changes do me in, and I syncope every time. My high school (this was early 90's, so no one knew much of anything about wny this was happening, and my PCP at the time eventually just gave me a note excusing me from gym until we were done with aerobics) did aerobics for a whole quarter, and by the time we were 5 minutes into the routine the ambulance was on its way to collect me! I also found, much, MUCH later (as in 8 months ago!) that I have EDS, and I am sure that plays a large role in my exercise intolerancve as well.

Sandy

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