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Does non-Hyper POTS involve norepinephrine release?


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Does non-Hyper POTS still involve the release of excessive norepinephrine when standing? My understanding was that with regular POTS the nervous system is receiving the message that there’s not enough blood going to the brain, so more Adrenalin will be released to trigger the vessels to try to constrict further. Probably repeatedly. Is that right?

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Hello @Elizaangelica - the question of the mechanisms behind different types of POTS is difficult to answer. There are so many different ways the ANS can malfunction! There is low-volume POTS ( the ANS responds to low volume of circulating blood ), POTS caused by EDS ( the blood vessels cannot constrict adequately due to being too elastic ), neuropathic POTS ( like SFN etc, where the nerve endings communicating within the ANS are defunct ), HPOTS, where the ANS responds to different triggers by dumping norepinephrine and causes excessive vasoconstriction, and many more. Many causes in POTS are genetic, others are a compensatory reaction. Here are 3 articles from our website that might help clear it up for you: 

Hyperadrenergic POTS (hyperPOTS) An overview of a POTS subtype - POTS - Dysautonomia Information Network (DINET)

POTS: An overview - POTS - Dysautonomia Information Network (DINET)

What are the Mechanisms of POTS & other forms of Dysautonomia? - POTS - Dysautonomia Information Network (DINET)

5 hours ago, Elizaangelica said:

My understanding was that with regular POTS the nervous system is receiving the message that there’s not enough blood going to the brain, so more Adrenalin will be released to trigger the vessels to try to constrict further.

This is ONE explanation of what happens in SOME cases of POTS. What you refer to as "regular POTS" is most likely the most common type - the vessels are unable to constrict properly and therefore the body is unable to circulate blood correctly - this causing tachycardia and other POTS symptoms. This is usually caused by excessive vasodilation. The hyperadrenergic subtype is commonly caused by sympathetic overcompensation, meaning that in response to a malfunctioning within the ANS the sympathetic NS overreacts by dumping adrenaline. 

This is a very confusing and overwhelming issue, even to most physicians. It takes time to make sense of it all and that is why it is so important to be in the care of a knowledgeable specialist. Most cardiologists ( who are the Ones most frequently seeing POTS patients due to the symptoms of tachycardia, chest pain and syncope etc ) are not knowledgeable in the different subtypes, and there is not a standard treatment for ANY of the types of POTS. This is why treatment is frustrating, and usually requires trying out different meds until the right one is found. I have HPOTS but did not respond to many of the typically used HPOTS meds, so there was a lot of trial-and-error involved in finding the right combination. But what counts is that I now am relatively stable on my meds ( albeit not cured ), so we just have to be brave, kiss a lot of frogs and not give up!!!!

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9 hours ago, Elizaangelica said:

Does non-Hyper POTS still involve the release of excessive norepinephrine when standing? My understanding was that with regular POTS the nervous system is receiving the message that there’s not enough blood going to the brain, so more Adrenalin will be released to trigger the vessels to try to constrict further. Probably repeatedly. Is that right?

This makes total sense. I think this is what is happening to me. When I actually do get blood flow to my brain which happened on accident months ago in the ER, all the OCD, anxiety, fatigue, brain fog, went away and I felt better than I had in years and slept well that night. It was a combination of things they did and some things that were accidental but it showed up that that was the primary issue. 

Thanks @Pistol you're very knowledgeable and helpful. Good information to print out. 

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Hypo-POTS, at least the way I understood it, means that norepinephrine was either not released enough or it was released enough but your receptors were broken and not receiving the signal well. My norepinephrine levels were fine, but I had hypo-POTS at the time. They gave me meds to increase norepinephrine but the levels got too high. I still fainted. It was thought that my receptors were damaged. This was not something that they could test for. It was just a theory. 

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And then there is neurally mediated hypotension (which I have) where there is no rise in HR, just a fall in BP which also makes you faint. And there seem to be subtypes of NMH also, as my parasympathetic nervous system is in overdrive so I respond well to medication that increases norepinephrine in the synapses. I think many call all types of orthostatic intolerance POTS, but this is not true and in order to treat the patient you need to dig down to the subtype.

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7 hours ago, Sushi said:

I think many call all types of orthostatic intolerance POTS, but this is not true and in order to treat the patient you need to dig down to the subtype.

Well said, @Sushi!

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On 6/12/2021 at 12:30 AM, KiminOrlando said:

Hypo-POTS, at least the way I understood it, means that norepinephrine was either not released enough or it was released enough but your receptors were broken and not receiving the signal well.

@KiminOrlando - I have never heard of this term before. Is this a new classification? 

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