haugr

https://gothamist.com/news/new-yorkers-with-long-haul-symptoms-are-upending-the-narrative-about-covid-19

@Derek1987 Have you had your testosterone levels checked by chance?

An ACE2 deficiency can lead to low renin and is a known cause of hyper pots.  The deficient ACE2 ends up leading to a high amount of angiotensin II in the blood stream, which ultimately causes the kidneys to lower their renin production.

Zoloft has been a positive for me.

I get that too.  I noticed with me that my ears got bright red as I was coming down from an hyperadrenergic episode.  I have a theory that it happens after severe vasoconstriction as the blood vessels dilate and blood flow increases.  I have seen a couple of papers suggesting Red Ear Syndrome is the same as Erythromelalgia of the ears.

I think that there is a good chance that those of us with with POTS caused by an ACE2 deficiency are coronavirus resistant since coronavirus infects cells by binding to the very thing that is broken in us.  The outlook might even be better for those that are taking Losartan to treat their ACE2 deficiency since that is a med that is currently being used in clinical trials as a coronavirus treatment. 

Having said that though, I am not taking any chances.  I am staying as quarantined as possible until a vaccine is out.

23 hours ago, Philipp said:

I am currently waiting for my Angiotensin II antibody Test. I have confirmed antibodies against a1 and m4 receptor

Where did you have those tests done?

I am not really sure.  Julien Stewart had reported some positive results from increasing anti-oxidants though.

I wouldn't.  Too many non-gaurantees for such a permanent decision IMHO.

No kidding.  I wish these tests were commonly available.

I found that paper about high angiotensin II levels in some potsies and its effects on renin: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4511483

A subset of POTS patients with increased vasoconstriction related to decreased bioavailable NO (nitric oxide) have decreased blood volume

Ang II reduces bioavailable Nitric Oxide

Ang II can increase the release of noradrenaline (norepinephrine) from ganglionic and postganglionic sympathetic nerves

Ang II promotes oxidative stress by causing the formation of superoxide radical through its effects on NADPH oxidase.  The interaction with superoxide reduces the bioavailable Nitric Oxide

Ang II is part of a control loop with feedback inhibition of renin production. Thus increased exogenous or endogenous plasma concentrations of Ang II suppress the release and expression of renin

On 7/13/2019 at 9:31 AM, PJPW said:

Curious if anyone can suggest things to help. DD was dxed with high epinephrine but not norepinephrine. So her Dr said she does not have hyperpots. What we do know is her blood pressure and heart rate are high an upon standing...goes higher. Current med is propanalol. She was tried on the clonidine patch at the lowest dose possible and she was dizzy upon standing and by day 4 so fatigued that she said her vision was blurry. Dr said to remove the patch and restart the propanalol. A few years ago she was started on florinef and did not do well at all. Blood pressure went up and she would go into a secondary seizure for around 20 minutes.

 

Just hoping someone has input

It makes sense to me that clonidine would have those negative effects since clonidine primarily suppresses norepinephrine instead of epinephrine.  An alpha-beta blocker would probably help get the blood pressure down.  Might want to also get tested for a pheochromocytoma if it hasn't already been done.

I've never heard of infections being associated with pots.  The others I think could possibly be attributed to high adrenaline.  I would recommend looking up the symptoms of a pheochromocytoma since it will give a good description of what happens when your adrenaline gets out of control.

I think that mine is genetic.  I have 4 biological siblings and 2 of them, while not officially diagnosed, are convinced that they also have it.  My sister had been dealing with what she thought were panic attacks her entire life until she did the poor mans tilt table after I was diagnoses and she turned out to meet the criteria.  Since then she has been pounding the sports drinks which has helped her immensely.  My brother has really high blood pressure and low testosterone that he was diagnosed with in his late 20s.  He also is on a high salt diet and lisonopril (which reduces Angiotensin II).  I have another cousin in her early 20s that was passing out from time to time until she was put on a high salt diet.  I should probably submit myself and my family to a genetic researcher

That actually sounds like the perfect summer to me

5 hours ago, bombsh3ll said:

How do you get around the RAAS suppression caused by high salt ingestion, when this system is likely already not working properly to begin with? 

B xxx

What causes this particular form of hyper pots (or Low Flow POTS as Julien Stewart calls it), is that there is too much Angiotensin II in the blood stream because the ACE2 is broken and fails to catabolize the Angiotensin II properly into the lesser forms of Angiotensin known as Angiotensin 1-7.  The kidneys then have a feedback loop that suppresses the release Renin when Angiotensin II levels are high.

So... why does salt help?   Well, the main goal is to get your Angiotensin II levels down to a tolerable level.  Salt and extra fluids raises your blood volume which leads to a state where your RAAS doesn't even really need to activate which allows your Angiotensin II levels to finally decrease as it gets slowly gets converted to Aldosterone which actually ends up lowering your blood pressure.  The raised blood volume also gets the other POTS symptoms under control.  Julien Stewart also recommends Losartan as a way to suppress the effects of the high Angiotensin II levels.

Salt with hyperpots is tricky.  You pretty much have to salt supplement if your symptoms are due to hypovolemia, but if you take too much though it will cause your bp to go higher, from what I understand.  In your case, I would guess the frequent urination is a pretty goid sign that you are likely hypovolemic.

@Outaker I am actually so glad to hear that you were able to get confirmation.  I know it has been a long and drawn out battle for you.  Were you able to find a local clinic to do the standing vs suppine catechlomines test?

Clonidine FTW!  That stuff is known to make you sleepy and suppress the release of adrenaline.

On 2/18/2019 at 7:29 PM, RachaelLee56 said:

What is the RAS club? 

Agreed @Outaker, sounds like she could be a member of the club.  lol

@RachaelLee56 what he's referring to is a known cause of POTS that results from a dysfunctional RAAS.   Here's a guide that I wrote up about it:  http://hyperpots.blogspot.com .  

I have found that the best descriptions online can be found from the descriptions of the symptoms of a pheochromocytoma since they can present in a very similar manner.

Paleness is a symptom of what Julien Stewart refers to as low flow pots that is caused by severe vasoconstriction.  I havent seen anything in the literature about black eyes, although I did notice from my own experience some discoloration and sunkenness around and under my eyes that made me a bit self conscious when I was highly symptomatic.

I am so sorry man.  Those docs really dropped the ball.  I cant even begin to imagine what you must be going through.

On 9/12/2018 at 12:32 PM, bombsh3ll said:

Thanks for sharing, do you know if there is any way to watch this online for those who cannot physically attend? Also which one is your doctor?

B x

I don't think that it's going to be live broadcast, although I know that this group of doctors have posted YouTube videos of their lectures before, so it's possible that they do it again.  Coleby is my doctor.

In case anyone is interested, there is an upcoming POTS conference on September 29th in Salt Lake City, Utah.  One of the doctors that is speaking is the doctor that treated me and got me back up on my feet.

http://www.dysautonomiainternational.org/page.php?ID=268