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Angiotensin Ii


jangle

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Any specific symptoms that your son experienced that might make him stand out from the average potsie? Cold all the time? pooling? bad reaction to beta blockers? etc.

Danny was not able to tolerate any vasoconstrictors - midodrine, mestinon, adderall - nor beta blockers. No relief until we hit on Losartan. Dan is hypovolemic but has high albumin. It seems like most Potsies have low albumin, but I don't know how much that matters. He used to be cold a lot but that has improved along with the rest of his symptoms. I don't think has pooling. Basically, he deals with fatigue, poor sleep quality, dizziness, headaches, nausea, brain fog, but has seen some improvement in everything except sleep quality.

I think that the real clue to Dan is the fact that he has low or no haptoglobin. Haptoglobin is a positive acute phase protein that binds

free hemoglobin and removes it from the circulation to prevent kidney injury and iron loss following hemolysis. We can't figure out why Dan is deficient in haptoglobin, because he is not anemic, does not have hereditary spherocytosis, does not have sickle call anemia (we're caucasian). In light of all the things he DOESN'T HAVE, the hemotologists we've consulted have dismissed this anomaly as unimportant. But I believe they're wrong. There's growing research out there that "naked hemoglobin", that is, hemoglobin without haptoglobin, is toxic and IS A NITRIC OXIDE SCAVENGER. We are searching for a doctor (anywhere in the country) who has an understanding of this and is willing to evaluate Danny. We may have caught the attention of a doctor at the U. of Pittsburgh, but like everything else in the crazy world of POTS, getting an appointment is a long slow process.

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Lenna,

Do you know what his renin/aldosterone levels are? I think I've asked this before - but, can't remember. Sorry, if I have. Does he have high salt levels? What's his potassium levels?

I can't tolerate any of those meds either - but, the Lorsartan made me feel like I was having a heart attack. And I don't need to vasoconstrict my veins either. I'm one of those odd ones and no one can figure me out. Trying to collect all the info I can. Thanks!

Issie

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Issie, you asked but I don't think I ever answered. Sorry. His renin/aldosterone levels were normal. (it's been a while since they were tested.) His salt levels and potassium levels are tested every few months and they are consistently normal. Losartan and Florinef might balance each other out with the Postassium.

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Issie, you asked but I don't think I ever answered. Sorry. His renin/aldosterone levels were normal. (it's been a while since they were tested.) His salt levels and potassium levels are tested every few months and they are consistently normal. Losartan and Florinef might balance each other out with the Postassium.

Okay, that would make sense. I wonder if because my renin and aldosterone levels are nearly non-existent - if lowering the angiotension II levels (If they were high, in the first place - don't know) was the wrong thing to do - because maybe with those levels already being nearly non-existent - the angiotension may not need to be lowered - it could have been high (if it is) for a reason. Maybe something to do with the autoantibodies. Maybe it's keeping potassium levels in check. But, if the chain of breakdown in the kidneys (renin, angiotension 1, angiotension 2, aldosterone) is how it goes - than it's not likely that an elevated angiotension level would be coming from the kidney chain of events because that would be low too. (low renin on one end and low aldosterone on the other - makes the inbetween low too) So, if that's the case - then where would the high angiotension levels be coming from? They can be produced in the heart and liver. So, maybe if angiotension is high and someone's renin and aldosterone levels are low - the dysfuction of the paradox of high angiotension could be from somewhere else in the body. But, WHERE? (I hope people are able to follow my rambling line of thought.) Just trying to make this make sense. I was so sure that the Lorsartan would work for me and when it didn't - I really couldn't figure that one out. There seems to be a connection with the autoantibodies to ACE2 and connective tissue disorders (possibly EDS) which I have also. Not sure how to tweek this.

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Issie, you asked but I don't think I ever answered. Sorry. His renin/aldosterone levels were normal. (it's been a while since they were tested.) His salt levels and potassium levels are tested every few months and they are consistently normal. Losartan and Florinef might balance each other out with the Postassium.

Okay, that would make sense. I wonder if because my renin and aldosterone levels are nearly non-existent - if lowering the angiotension II levels (If they were high, in the first place - don't know) was the wrong thing to do - because maybe with those levels already being nearly non-existent - the angiotension may not need to be lowered - it could have been high (if it is) for a reason. Maybe something to do with the autoantibodies. Maybe it's keeping potassium levels in check. But, if the chain of breakdown in the kidneys (renin, angiotension 1, angiotension 2, aldosterone) is how it goes - than it's not likely that an elevated angiotension level would be coming from the kidney chain of events because that would be low too. (low renin on one end and low aldosterone on the other - makes the inbetween low too) So, if that's the case - then where would the high angiotension levels be coming from? They can be produced in the heart and liver. So, maybe if angiotension is high and someone's renin and aldosterone levels are low - the dysfuction of the paradox of high angiotension could be from somewhere else in the body. But, WHERE? (I hope people are able to follow my rambling line of thought.) Just trying to make this make sense. I was so sure that the Lorsartan would work for me and when it didn't - I really couldn't figure that one out. There seems to be a connection with the autoantibodies to ACE2 and connective tissue disorders (possibly EDS) which I have also. Not sure how to tweek this.

THAT! is a very interesting question. One I hope we do not have to answer, sort of like solving an equation like (x^3+SQRT(EXP(x^2+SQRT(x))) * Log(x) * 0 = 0

If that 0 wasn't there, that'd be really difficult to solve for x. But hopefully we won't have to answer that question, hopefully we can just find a medicine that ups ACE2 levels and gets us better without ever having to know the gory details. (In this example the medicine would have the effect of putting the 0 in the equation)

Otherwise we're in for some rough science.

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Jangle, I finally went and looked up this stuff up. Something noteworthy is the effect of enzymes. Since we are talking about the ace2 precursor to angiotensin ii. Essentially, the role of an enzyme is to reduce the energy required to make a chemical reaction occur. In this case the amount of energy required to compose angiotensin ii out of other molecules. Now if ace2 is high you can expect higher levels of angiotensin ii etc I am curious about angiotensinogen and its globulin precursor.

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Lemons,

But, what we are suspecting is there are autoantibodies to ACE2 causing them to be somewhat ineffective. Therefore, we need to up them, not decrease them. But, possibly lower angiotension II. (Am I still on track guys? I'm starting to get fuzzy headed.)

The precusser to angiotensigen is renin - the first line in the kidney cycle.

(Did you get my earlier messeage about wondering if you plan to address this and if you want me to take info in before you get here?)

Issie

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Lemons ace2 converts angiotensin ii to 1-7. So high ACE2 would mean low angiotensin ii. Conversely low ACE2 would mean high angiotensin ii. Lissy that is interesting I haven't thought about the potential of antibodies to interrupt in some way the function of ACE2. It might not be a binary thing (either you have normal ACE2 or you don't) but rather having abnormally functioning ones. That would make treatment much different.

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If this is an angiotensin ii or ace2 deficiency, why did I become orthostatic in my 20's? This leads me away from gene expression because if it were a defective gene, then the symptoms would have been present since birth. Unless, we are talking about a mutation that is deficient and continuing to copy itself.

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Not all genetic defects have effects from birth. SOme There are plenty of circumstances where a less pronounce polymorphism or gene defect does not come into effect until later in life.

Celiac Disease is an example, etc. A strong genetic predisposition gives you it from birth. A less pronounced disposition arrives usually in late teens early 20s.

Also consider the possibility of epigenetic changes to gene expression, inflammatory cytokines altering the expression of the gene and the possibility of an autoimmune mediated reaction. There could also be something genetically or acquired that is wrong with the ang II receptors, causing ang II to increase to compensate.

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