Labs:angiotensin 2,aldosterone, Renin

[POTLUCK]

I got my lab results for these 3 back. They were done while on Inderal 140 a day, but prior to adding Losartan to it.

Angiotensin II 13 ( Low. In normal range ) ( lab < or = 86 norm.)

Aldosterone 4 ( In normal range ) ( lab < or = 28 norm )

Plasma Renin Activity ( 0.84 In normal range) ( lab 0.25-5.82 ng/ml/h norm.)

Angiotensin II is not elevated as it often is in low flow POTS (89 avg in Dr. Stewarts study), in fact it is lower than the average normal in Dr. Stewarts study (32.) Renin (PRA) was not low as it often is in low flow POTS, in fact it is awfully close to the (.90) average for normals that Stewart found. On graph of correlation between renin and aldosterone they correlate on line.

http://www.nymc.edu/fhp/centers/syncope/angiotensin_in_pots.htm

These data do not suggest low flow POTS. It could be...

1. I do not know if being on B-blocker can affect.

2. I was not impressed that the lab had any experience doing this.

3. Stewart did find some low flow POTS patients with low angiotensin

Overall though, these labs do not support my theory of having low flow POTS, which does not make me happy, as I would like to see the picture come together not fall apart.

My free fractionated catecholamines Lying and standing are pending, but the B-blocker can definately affect those results- though to what degree I have no idea. I would have preferred to have them done off B-blocker when I had my tilt.

The Losartan has not made me any worse and possibly is helping. I am currently taking 25 BID with upward titration over time planned. I am pretty sure it has lowered the BP lying and standing a little.

Although I hope the data is useful to someone, this post is also to vent that the Angiotensin did not come back high and support the low flow theory.

Thanks for listening/ ( reading )

[issie]

Bummer, just when you think you have it figured out. I've had this happen so many times and then you don't know what direction to go in. I feel the frustration. But, at least you know now. It's a whole lot of test and a whole lot of questions and as each one gets it's answer - it just adds more to the entire picture as a whole. It's part of the complicated process. You're getting some answers - just not the ones you'd hoped for. Hang In There! It will come together better for you, with time.

Issie

[bellgirl]

I believe you are right to think that the beta blocker could affect your lab work, because it does affect your kidneys. If you were on the Losartan, too, before your lab work, it would definitely skew the results. I know for sure!! That's why I can't have that done...I've been on Losartan for at least 10 years, and an ACE inhibitor before that...Hope you continue to get some answers. The Losartan works well for me with Bystolic, long acting BB.

[ramakentesh]

Even on a lot of meds that ang II is very low. Have you considered net deficiency as a possible issue? Postural hypertension and all.

[ramakentesh]

In net deficiency there might be increased peripheral dopamine stimulating kidney's to release too much salt during orthostatic stress. Also capillories might be allowing plasma to leak into the stomach area. Alpha 2 receptors may be faulty and these are important for stomach vasoconstriction . But cerebral autoregulation might be the biggest problem in most.

[POTLUCK]

In net deficiency there might be increased peripheral dopamine stimulating kidney's to release too much salt during orthostatic stress. Also capillories might be allowing plasma to leak into the stomach area. Alpha 2 receptors may be faulty and these are important for stomach vasoconstriction . But cerebral autoregulation might be the biggest problem in most.

I do not know much about it. My catecholamines are PND. ( Done on 140mg Inderal-best I could get done as hard to get someone to order it. ) Will they suggest one way or the other? Is there testing for it? Net deficiency is the thing discovered by the Vanderbilt people & published in NEJM around 2000 isn't it? I thought they only found a handful of people with it, and it did not pan out to be a big cause for POTS??

[issie]

I just bumped an old thread on NET dysfunction. Even though there may not be a whole lot of POTS people affected by this dysfunction - there are some and it would merit consideration. If, it is the reason and tweaking things in regard to that dysfunction - may be a solution to some peoples issues.

One thing about it POTLUCK - if your noriepi levels come back high and the test was done correctly - you can assume that you would qualify to be with us HyperPOTS people. Especially since you demonstrate the high bp's that a good many of us have with high NE levels. (I can't remember if you've already gotten your results yet.) It will be interesting to see what the levels are with you being on such high doses of propranolol.

Issie

[ramakentesh]

There was a study from Australia that suggested that nearly all POTS patients tested had no NET - because of epigenetic gene silencing rather than an actual genetic fault. Its a bit murky but they did find reduced experession of NET in the forarm veins of all POTS patients tested.

Problem is that ang II might effect NET function or expression and in the neuropathic POTS there was also reduced NE reuptake recorded.

The study on reduced MIBG reuptake suggested it showed cardiac denervation - but its also possible it shows reduced NET function or expression alone.

Finally there was work looking for NET autoantibodies that was never published.

[POTLUCK]

There was a study from Australia that suggested that nearly all POTS patients tested had no NET - because of epigenetic gene silencing rather than an actual genetic fault. Its a bit murky but they did find reduced experession of NET in the forarm veins of all POTS patients tested.

Problem is that ang II might effect NET function or expression and in the neuropathic POTS there was also reduced NE reuptake recorded.

The study on reduced MIBG reuptake suggested it showed cardiac denervation - but its also possible it shows reduced NET function or expression alone.

Finally there was work looking for NET autoantibodies that was never published.

Rama,

I am not following you on this. If everyone may have decreased NET than what is the value of considering if I might have it? Second you mentioned the decreased stomach vasoconstriction thing in regard to alpha 2 receptors. Does this go with Dr. Stewarts Regular flow POTS? do you go by Dr. S. categories? Lastly you mentioned the neuropathic POTS, are you seeing this as a different entity from hyperadrenergic POTS, because at times you have suggested all POTS patients are hyperadrenergic. I suppose what I am asking overall is how are you subdividing POTS patients. To my way of thinking, some aspects of POTS are opposites- like patients who have low flow and patients who have high flow. Some patients can not stand long without passing out , and I have never passed out. I do not use the word presyncopal for this reason. It also seems to me that coming up with ways to divide things is clearly helpful with treatment, rather than simply trying meds. You appear to have done a great deal of research and are obviously a bright guy and I am wondering what your thoughts based on all of this are.

[ramakentesh]

Im just demonstrating that a lot of the research is murky.

I meant that all forms of POTS have hyperadrenergic features in terms of subjective symptoms - feelings of anxiety, jitteriness, etc.

I think this is probably the most accurate description:

1. Low flow states/vasoconstrictive - ang II, Net deficiency (maybe) and hypovolumia.

2. neuropathic POTS/high flow/EDS - peripheral poolers

3. Other - parasympathetic withdrawal, increased NO, autoregulatory problems, etc.

Problem is that if you try and apply any of the catagorisations in the research and on websites to patients they never fit properly. I and most have features that kind of blurr in between catagories.

I guess that postural hypertension is useful in that it suggests a overconstricting problem but it could be compensatory.

Its all confusing and certainly still being debated.

[POTLUCK]

Thanks,

I believe I follow you. I appreciate your noting the categories. What do you think about Stewart's "regular flow" category that is supposed to have increased NO with increased splachnic pooling but not feet pooling.

I ask specifically because I figure I am not category 2 above, as I can be standing and staring down at my blue or white ice cold toes, and I am never looking at pooling in my feet or toes. Also, I do not faint, and my BP does not drop on standing. But I could be "normal flow" type with splanchnic pooling.

[Chaos]

Potluck- I think several of us on here find it hard to pigeon hole ourselves into any one category, either Stewarts or otherwise. Personally I think I move between Stewart's categories depending on the day. I have been diagnosed with neuropathic POTS but with hyperadrenergic component. To paraphrase Rama- it's clear as mud. LOL

[ramakentesh]

If i was in a catagory of Julian Stewart I would be either Normal flow or low flow - probably leaning towards teh later. It also contains NET deficiency and other causes were low NO is suspected.