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I think I understand what you're trying to say Rich. If there was true high NE then it would be high all the time - like with a pheo. If there is a transporter issue -and that is what they are connecting to POTS - then why is it there only with upright standing posture and not like a pheo and there all the time. Is that what you're trying to say? I'm just trying to understand what you're trying to understand about NET.

Issie

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There are studies that talk about how/why this is happening. You have to read the full study though. I'll try to take a look around here and I'll post them here if I find them. There's that one about mice and the healthy subjects they induced POTS in, that I've already posted in the other thread. There are also others though I've come across that the issues are only when standing because of sympathetic stimulation or something like that. When you sit down, the parasympathetic nervous system kicks in, so there is less NE traveling through the synapses any way thus the decrease in NE clearance doesn't become an issue. Hopefully I'm making sense and not botching this...

From this study:

"Second, although norepinephrine spillover and clearance are similar in patients and normal subjects when supine, spillover fails to increase and clearance actually decreases with upright posture in patients."

"Supine norepinephrine was also greater in patients. Although the increase in norepinephrine spillover with standing was similar in patients and control subjects, the decrease in clearance was greater in patients than control subjects, indicating that much of the increase in plasma norepinephrine was due to a decrease in clearance."

Rama, the thing is NET deficiency = higher than normal NE levels almost like Pheochromocytoma. The difference is the researchers that link NET def to hyper pots mean that this NET deficiency only occurs while standing. Read this and you can see the connection http://www.ncbi.nlm....pubmed/17102094

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This NET topic is one I've been interested to understand but this thread and even links are way beyond my level of comprehension. Can someone help me understand this at a milk and cookies level?

When I went to Cleveland clinic they noted my NE was elevated upon upright tilt. I got weak and started to faint so the TTT was stopped- my NE was up to almost 800. Does that related?

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This NET topic is one I've been interested to understand but this thread and even links are way beyond my level of comprehension. Can someone help me understand this at a milk and cookies level?

i second this. i struggle to understand a lot of things posted here, this being one of them. and, i don't have a lot of free time to research. <_<

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You guys, don't feel rained on - (southern expression for feeling alone with something). When we all started with our understanding - we understood nothing. With a lot of time and reading, things will start to make sense and click.

When you have high NE levels - depending on which clinic you go to - you are considered HyperPOTS. Some docs treat people who are HyperPOTS with different meds.

You can do a search on NE and it will bring up all of our discussions for at least the last year. The more you read - the more you will start to understand what we're talking about. But, really - what we think we understand today - could very possibly be changed tomorrow. Science and medicine is advancing and we have to be open to other ideas and new explanations and not be set that how we think we understand something today is set in stone. Cause, it very well could crumble into rubble.

Issie

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Hey sorry for all the technical terms.

Catecholamine (Epinephrine (adrenaline), Dopamine and Norepinephrine (Noradrenaline)= the messengers in the body that act on behalf of the Automonic nervous system (ANS). If a big scary bear was 10 feet in front of you, your ANS would take over command and send these messengers out to different parts of your body to help you cope or run and escape the bear. It heightens all your senses (dopamine) and can send your body into hyperdrive (your heart rate would go up for example, mostly because of adrenaline and noradrenaline). So what the docs are trying to see is why some of us have high norepinephrine levels when we are upright, because that is not normal if there is no stress or attack..

Norepinephrine Transporter= is the system the ANS uses to keep our norepinephrine levels normal when we arent attacked. So by having high upright levels the 1st suspect is the regulating device in our bodies (NET). There could be many other suspects besides that. For example a computer might malfunction because of a software error or the hardware is getting old or it may be attacked by a virus or maybe the hardware is malfunctioning because a virus attacked it... So even if we find NET issues, what caused it?

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Rama, the thing is NET deficiency = higher than normal NE levels almost like Pheochromocytoma. The difference is the researchers that link NET def to hyper pots mean that this NET deficiency only occurs while standing. Read this and you can see the connection

incorrect. the Jens Jordan and a few other studies showed normal NE levels with NET inhibition, although in the original proband study NE was elevated. You might expect increased NE but the problem is that NET inhibition in the brain supresses sympathetic outflow via alpha 2 receptors! Having read all the studies on NET deficiency I can guarantee you that none of the researchers are suggesting that NET is deficient only when standing. its a protein imbedded in the sympathetic ganglia and it cannot vary that quickly. In fact since all the studies suggest gene supression either through mutation or epigenetic supression this would mean that the NET protein was supressed chronically rather than only when standing.

Once again I would suggest reviewing specific research that relates to POTS and that incorporates contemporary observations.

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