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Standing Ne Levels


nunntrio
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I think he states that POTS patients often have NE > 600 due to sympathetic activation. I don't think this is required for a diagnosis by all POTS clinicians. I do see what you are talking about in the criteria table though. My last tilt showed a HR increase over 30 bpm, but my standing NE level was just under 300. The doctor did tell me that he can't remember the last time he saw a POTS patient with such low catecholamines. They thought the mechanism may be parasympathetic withdrawal, not necessarily a high level of catecholamines if this makes any sense. I have improved over the past 2 years drastically, and I have gone from hypovolemia to hypervolemia, but I still have symptoms. At one time, my seated catecholamines were almost 500.

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The diagnosis criteria is slightly different everywhere and it really depends on what hospital/facility/doctor you see. Some hospitals categorize hyperadrenergic POTS for anyone with standing NE levels above 600. Obviously this means that being >600 is the exception rather than the norm...but that's just my opinion!

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So, having had a seated blood draw and testing just norepinephrine levels - that was above 600. I'm guessing that definitely qualifies me as certified hyper POTS. I have all the symptoms of it but not officially said Hyper POTS. None of the meds for POTS has worked for me and that could explain why.

But, what does it mean if dopamine levels are low? Norepinephrine can be derived from dopamine. How can one be too high and the other too low?

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At places like Vanderbilt and the IEEM in Dallas, they insert an IV line, have you lye down for 30 minutes before the supine draw, and handle the blood sample in a very specific way. NE levels can be high from a regular blood draw from the pain of the prick. Dopamine normal reference levels are normally low or non-existant, but there is obviously enough if we have EPI and NE since they are derived from dopamine.

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Normal dopamine levels are 0-20 pg/ml, and labs will often report results as less than 20 pg/ml.

The seated NE I had drawn at my local lab was higher than my standing NE level. The local lab result is as good as trash because it was not collected under proper protocol.

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This is an interesting thread. From what I can gather, according to Dr. Raj NE levels over 600 mean POTS, and over 1000 qualify as hyperadrenergic POTS. Mine were taken as TXPOTS described in an autonomic lab up here in Canada that was recommended by Dr. Raj. My supine NE after resting quietly for a while was abnormally low, but after ten minutes of tilt it was nearly 1700 - they decided I am hyperadrenergic POTS, but I don't seen to have high blood pressure. I can't remember the exact numbers right now, but my adrenaline levels after the 10 min were 26 times the upper level of normal (no wonder I feel weird sometimes).

It seems important to remember how different we are in some ways, and I really appreciate it when people share things like this. I keep feeling guilty about having not cured myself by being active, but maybe what works for one person or group of us may not work the same/as well for others (although exercise overall seems to be helping, despite the fact that after each exercise session I get sicker).

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Thanks for all the replies. I also thought that >600 was just for the hyper diagnosis of POTS. It seems there is not a complete agreement amongst the expert medical facilities for a clear difinition of POTS. I like the idea of parasymapthic withdrawl may account for those of us that have low NE. I had all my testing done at Vandy and they are the one that gave me my POTS diagnosis. My standing NE levels via IV were all under 400 except for once when it did climb to 894 (yes they tested them 4 times). So according to this article I did not qualify for a POTS diagnosis. I have a feeling they are sick of me asking questions or I would email them to clarify. :) Still pretty sure I have POTS though as my posture study show a 40 bpm increase.

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All of this is very confusing and I even question NE > 600 automatically putting you into the Hyper POTS category. For me I have standing NE over 600 but I don't suffer from high BP upon standing at all. Mine were tested following proper protocol too! I think our adrenergic receptors can be ultrasensitive or insensitive, so a 600 for someone could be "normal" meanwhile maybe someone with levels of 400 can cause hyperPOTS like symptoms.

There are studies out there about the receptor sites and how they change according to thyroid function, so I think this is likely with POTS too. I'm just me thinking out loud and realize this isn't really going anywhere!!!...haha

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Exactly Dana...

My standing NE taken by a very experienced autonomic testing facility with a research assistant and 2 cardiologists present was not even 300. My blood pressure was sky high, and my legs were trembling. I have HYPER POTS symptoms, but completely normal catecholamines. Dr. Levine thought parasympathetic withdrawal, but I think a receptor supersensitivity is a great thought. In fact, this happens in the pharmacy world all the time. An example is benzodiazepine use. After taking benzos long term, the GABA receptors are downregulated. So, when a patients stops taking the benzo abruptly, they are at risk of seizures, trembling, panic attacks, etc... because the GABA (calming) receptors have been downregulated by the body.

Nunntrio,

Thanks for the interesting topic. I wish we weren't here discussing it at all.... but at least POTS can be intriguing.

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Well, I'm so sure that Hyper POTS is the type I have - actually, recently read they are considering another variant- a combination of the two. I would say that is where I fall in. I have times of low blood pressure and really, really high blood pressure. I always have severe tachy and pulse rates can swing just as wildly as the bp. From way too low to very high. So, I'm one more mixed-up mutt. Ha!Ha! It's very, very difficult to treat the extremes. So far, I'm not very successful with any of the meds I've tried. There are only a few that I haven't tried - clonidine and DDAVP and EPO. So, I do plan to ask to try these since I've tried everything else. I also think there is a mast cell problem involved with me. Oh, the joys of trying to figure it all out. We have to educate ourselves - so we can educate the doctors we seek out for help. We should get degrees and colleage credits for all this research we all do. I bet we know enough to have that little MD beside our names - at least on this subject - POTS.

Keep searching - we need all the knowledge and help we can get.

Oh, nearly forgot. It makes sense that there would be enough dopamine to make the norepi. But, dopamine is the feel good hormone. If it is all used up to make an over abundance of norepi. - couldn't the imbalance created cause more issues. I know it could cause depression and just generally a sense of unwell. When they thought I had Parkinsons and I tried sinement - it was horrible for me. Then I tried Wellbutrin - it made a difference for a short time - then it was equally horrible. I declined very fast on the regimine. Was also using Lexapro so that the seratonion levels wouldn't be too low because of the upping of the dopamine. Now, I test low on dopamine levels. I'm sure there has to be some sort of connection. Just don't know what. Any ideas?

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I've been researching this since you posted this and found an old link (that you participated in TXPOTS) that I've bumped. It has some good info in it about this subject. Mostly according to the new study - what I'm finding anyway is they want to see if high levels of dopamine contribute to POTS in relationship to receptors in the kidney and it's ability to affect sodium levels - (I have the opposite problem - low dopamine. Has my body intentionally done this on it's own?) Dopamine affects the vasodilation and salt effects in the kidney. There are certain meds that can affect the DA-1 receptor agonists - affects vasodilation and sodium transport and Selective DA-2 receptors - inhibit noriepi release and promotes vasodilation. Inhibits sodium reabsorption and regulation of sodium and excretion. (I've just done marathon reading on this and took notes as I did it.)

In hyper POTS it looks like if we could affect the DA-2 receptors and suppress the norepi and regulate sodium - that would be of GREAT benefit to us. There is also a connection between dopamine and aldosterone (which as you know - was another thing I researched rather intently). That could also account to the conclusion I drew that high salt loading (and question as to whether to use Florinef) and the connection between aldosterone - would NOT be so good - (especially in a Hyper POTS person).

Okay - my brain is on over load right now. One question - brings up another .... then another ....I'll let others chim in. Got to take a break.

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I don't know that a blood draw for dopamine or 24 hr urine collection translates well into the amount present at the kidney. Parkinson's patients have low dopamine in the brain, but the blood and urine tests are not useful for diagnosis, because dopamine levels are only effected in the brain. Plus, a dopamine level < 20 pg/ml is considered normal. They are manipulating dopamine levels peripherally with carbidopa, but I don't think they actually know what the specific kidney dopamine levels are.

Issie- Thanks for bumping the old post. Funny that we are still going round and round.

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Nunntrio,

Thanks for the interesting topic. I wish we weren't here discussing it at all.... but at least POTS can be intriguing.

No problem - The more I try to figure this out the more confusing it gets. I do like a mental challange but I am ready to have this one figured out. Hopefully it will happen in my lifetime.

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Dana - Do you have links to the thyroid function studies? I have a lot of hyper symptoms but low NE levles but I do have hpyothyriodism. It would be interisting to read.

Here is a study but you will note that people with hyperthyroidism have LOW (yes low) catecholamine levels even though they suffer from a hyperadrenergic state. Hypothyroid patients have higher levels of catecholamines, but it has everything to do with the receptor sites.

http://www.ncbi.nlm.nih.gov/pubmed/2189309

Here's another one that just says thyroid hormones play a role in the beta-adrenergic receptor responses to catecholamines.

http://www.ncbi.nlm.nih.gov/pubmed/6257196

If you type in catecholamines thyroid into google you'll find a lot more info.

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Here is a study but you will note that people with hyperthyroidism have LOW (yes low) catecholamine levels even though they suffer from a hyperadrenergic state. Hypothyroid patients have higher levels of catecholamines, but it has everything to do with the receptor sites.

http://www.ncbi.nlm.nih.gov/pubmed/2189309

Here's another one that just says thyroid hormones play a role in the beta-adrenergic receptor responses to catecholamines.

http://www.ncbi.nlm.nih.gov/pubmed/6257196

If you type in catecholamines thyroid into google you'll find a lot more info.

Thanks - Interesting. I will spend sometime reading about this.

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TXPOTS - from what I'm reading and how I'm understanding it - dopamine can have allot to do with the salt uptake by the kidney. They want to find out if lower dopamine levels cause a higher or lower uptake. I can answer that. My dopamine levels seem to be lower and my sodium levels are ALWAYS too high. That's without salt loading. So, why would I salt load - if my body's salt level is already too high. And also being hyper POTS - more salt could create a worse imbalance - not to mention raise the standing bp to an even higher number (when mine is already high at times). The dopamine can also affect aldosterone levels which in turn affects the fluid levels in the body. It appears that DA-1 (dopamine) receptors affect vasodilation and sodium transport and DA-2 (dopamine) receptors can inhibit noriepi release and promotes vasodilation, also inhibit sodium reabsorbition and regulate sodium excretion. So, dopamine in the kidney along with aldosterone and renin and the angiotensin II function are all intertwined. How much so, we don't know. So, those of us with hyper POTS and a high noriepi level - if there would be some way to regulate the DA-2 part of dopamine in the kidney - looks like that would help us. We all know that blood pressure issues can have some connection to kidney function and there is a strong relationship with this to circulatory and heart function. The dopamine also affects the vein contraction or laxity also (from what I'm understanding). HOW COMPLEX OUR BODIES ARE!!!!

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Just to clarify - POTS is defined as a 30 bpm increase in HR upon standing, and is determined w/o measuring norepinephrine levels.

Yes, true. And it appears that hyper POTS isn't always defined by norepinephrine level, since some people's levels are lower than what they are using as a guideline for that type of diagnosis. (Just an observation on my part.)

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