Annaliese

My bp goes really low at night such that my arms and legs freeze and get pins and needles. I also have episodes of tachy which i think is becuse of the low bp. Since getting ill my bp has always been the lowest whilst lying. I stopped taking beta blockers at night and these problems reduced.

What is the mehanism for excessive thirst and urination?

Thanks for posting Issie- i like the way your brain works. Yes, i googled estrogen and NO and was disappointed to find a postive rather than negative correlation between the two. The reason im thinkng estrogen is because of the autoimmne issues that seem to crop up a lot and also because dys is primarily a girl thing. Loads of dys women i know have had cystic boobs, ovaries and fibroids and have had hysterectomies. My psych also tld me that the breast cancer drug tamoxifen (an anti estrogen compound) has been used or trialed (cant remember what she said) to treat autoimmune disease. I think its tricky to work out if progesterone or estrogen improves or worsen pots. Estrogen we know helps us retain water so it apppears like it helps but perhaps only on that level. Short term Improvement in ortho tolerance with estrogen annoyingling doesnt exclude estrogen excess being the cause of pots in the first place. Why did pregnancy set off autoimmune processes in me? What happens in pregnancy- massive hormonal changes. Ive noticed that EDS woman with the worst symptoms of dys also have the worst cystic boobs and uterine problems. Perhaps EDS is linked to a supersenitivity to a particular hormone or something.... Who knows....my brain hurts! All i know is that the hormone link is very suspicious! Oh, btw, i saw an artcle on progesterone and pots, l will try and ind it again.

Lieze, im wondering if estrogen dominance is behind low flow pots. Especially if it causes mast cell activation. Effects of Estrogen Replacement Therapy on the Renin-Angiotensin System in Postmenopausal Women Abstract Background Oral estrogen replacement therapy (ERT) is known to stimulate the synthesis of angiotensinogen. The effects of such therapy on renin, ACE, and aldosterone are less clear. This seems noteworthy, however, since further activation of the system could be disadvantageous to postmenopausal women who replace estrogen in the context of heart failure, coronary artery disease, or hypertension. Methods and Results Estrogen status and components of the renin-angiotensin system were examined in a population-based sample of postmenopausal women and age-matched men. Renin was quantified immunoradiometrically, ie, independent of substrate abundance; aldosterone, angiotensinogen, and ACE activity were determined by standard methods. Renin levels were lower in women with ERT (n=107; 12.0±0.7 mU/L) compared with women without ERT (n=223; 16.6±0.9 mU/L; P=.001) or men (n=342, 20.5±1.5 mU/L, P<.0001). In contrast, angiotensinogen was higher in women with ERT (1.36±0.08 mg/L) compared with women without ERT (1.03±0.02 mg/L; P<.0001) or compared with men (0.97±0.01 mg/L; P<.0001). Renin suppression was seen with either oral or transdermal estrogen replacement (-30% and -31%, respectively; both P<.001). In contrast, the increase of angiotensinogen was limited to women taking oral estrogens (+58%, P<.001). Multivariate analysis revealed that these estrogen effects were independent of age, body mass index, blood pressure, and/or antihypertensive medication. Finally, only marginal differences between groups were observed for serum ACE activity and aldosterone. Conclusions Aside from a well-documented induction of angiotensinogen, ERT is related to a substantial suppression of renin, a phenomenon that might have received little attention because of widely used indirect measurements of the hormone.

I just looked up estrogen dominance and i have all those symptoms!

Issie, ignore my last Q, i looked it up. Is it possible the low renin and high angiotensin could be an estrogen dominance problem? See below.... Effects of Estrogen Replacement Therapy on the Renin-Angiotensin System in Postmenopausal Women Abstract Background Oral estrogen replacement therapy (ERT) is known to stimulate the synthesis of angiotensinogen. The effects of such therapy on renin, ACE, and aldosterone are less clear. This seems noteworthy, however, since further activation of the system could be disadvantageous to postmenopausal women who replace estrogen in the context of heart failure, coronary artery disease, or hypertension. F Methods and Results Estrogen status and components of the renin-angiotensin system were examined in a population-based sample of postmenopausal women and age-matched men. Renin was quantified immunoradiometrically, ie, independent of substrate abundance; aldosterone, angiotensinogen, and ACE activity were determined by standard methods. Renin levels were lower in women with ERT (n=107; 12.0±0.7 mU/L) compared with women without ERT (n=223; 16.6±0.9 mU/L; P=.001) or men (n=342, 20.5±1.5 mU/L, P<.0001). In contrast, angiotensinogen was higher in women with ERT (1.36±0.08 mg/L) compared with women without ERT (1.03±0.02 mg/L; P<.0001) or compared with men (0.97±0.01 mg/L; P<.0001). Renin suppression was seen with either oral or transdermal estrogen replacement (-30% and -31%, respectively; both P<.001). In contrast, the increase of angiotensinogen was limited to women taking oral estrogens (+58%, P<.001). Multivariate analysis revealed that these estrogen effects were independent of age, body mass index, blood pressure, and/or antihypertensive medication. Finally, only marginal differences between groups were observed for serum ACE activity and aldosterone. Conclusions Aside from a well-documented induction of angiotensinogen, ERT is related to a substantial suppression of renin, a phenomenon that might have received little attention because of widely used indirect measurements of the hormone.

I should also say ive actually been avoiding reading too many POTS papers because they keep repeating that quote someone said once about people getting POTS through pregnancy having the condition for life. Whenever i read that it makes me cry! I should quit being such a baby.

Issie, Im glad youve posted if ive got this mixed up! i havent been reading that many articles because i find my eyes cant cope with it. Instead ive been listening to med lectures on youtube and thought i had the renin ang system understood. So with regard to the paradox you are talking about, have they actually measured the renin and aldosterone in hyper pots people and found them to be low and measured the angiotensin II and found it to be high? I started taking florinef because over the last year my standing bp has lowered to the point now that its now too low (could this be due to adrenal burnout? ). The biggest worry for me though is my lying bp. It gets very low and it triggers histamine flushing and then tachy. Im worried im going to have a hypoxic stroke. I see what you mean about taking florinef and then my body learning not to make aldosterone. I have been wondering about that myself. I really want to be on no drugs at all to allow my body to try to sort itself out but at the moment i think its dangerous because of the potential stroke issue but alo because im starting to get neuropathy in my legs. I wonder if i would be better off on midodrine. During the day i dont care so much about the low blood pressure because at least i can monitor it, its the nights that are the problem. My legs are always freezing and i dont think much blood is getting down there. How are you at the moment?

I have suspected ive got MCAD for a while. I had serum tryptase measured and it was normal. But, just a few days ago i got a UTI and i got flush after flush after flush. This has to be a histamine response. I went asap to the drs and asked him to measure serum tryptase. Fingers crossed it will show up as it was bout 5 hours since the flushing. Perhaps you can try and induce flushing and then go and get a test? It is sooooooo frustrating knowing you have a disorder only to be ignored by the drs.

Hi Issie, the reason i think ive had chronic elevation of the renin angiotensin pathway is because ive experienced thirst and anxiety for over a year. When i started florinef the thirst went away. I basically think ive had low blood volume and that my high standing bp has been an overreaction to the low vol issue. I also seem to have histamine issues causing polyurea which i think has perpetuated the low blood vol. Im pretty sure im low flow POTS.

On a slightly different topic, I saw in some medical lectures that chronic elevation of the renin angiotensin system leads to cardiac fibrosis and hypertrophy and that this is why patients with congestive heart failure are given ACE inhibitors. I was starting to get scared because i have had low flow pots with all the hallmarks of chronically elevated renin-angiotensin. But then i found this : https://iris.Raised blood pressure, not renin-angiotensin systems, causes cardiac fibrosis in TGR m(Ren2)27 rats Abstract OBJECTIVES: Elevated systemic arterial blood pressure is associated with left ventricular hypertrophy and fibrosis. It has been suggested that both circulating and local myocardial renin-angiotensin systems play a role in mediating these responses. Here we describe the natural history of ventricular hypertrophy and fibrosis in the transgenic (mRen2)27 rat--a monogenetic model--which has a high tissue expression of the murine renin transgene, and suffers severe hypertension. We further explored the relative contribution of both hypertensive burden and circulating and tissue renin-angiotensin systems to the fibrotic process. METHODS: The transgenic rats were treated from 28 days old with (1) a hypotensive dose of the ACE inhibitor ramipril which inhibited both tissue and circulating ACE activity, (2) the calcium antagonist amlodipine, or (3) a non-hypotensive dose of ramipril which inhibited about 60% of tissue ACE activity with little effect on circulating ACE. Normotensive Sprague-Dawley rats were used as controls. RESULTS: The transgenics developed left ventricular hypertrophy along with perivascular and interstitial fibrosis which became progressively worse up to 24 weeks of age. Both the high dose of ramipril and amlodipine prevented the hypertrophy and fibrosis, whereas tissue ACE inhibition without lowering blood pressure had no effect, and actually led to a worsening of the fibrosis by 24 weeks. CONCLUSIONS: These results suggest that the development of left ventricular hypertrophy and fibrosis in the transgenic (mRen2)27 rat are regulated by blood pressure and not activity of the renin- angiotensin systems and that progression of fibrosis at 24 weeks involves a mechanism unrelated to local renin-angiotensin activity

Ah, Ok. Thanks. Ramakentish there's one thing ive been meaning to ask you. In hyper pots where you tend to get polyurea, what is the mechanism for this? I dont understand it because the sympathetic nervous system is going crazy -the flight and fight response tends to stop urination so why all the peeing? I used to have high standing bp (and hence i think i had hyper pots) but over the year its gotten lower and lower but the one thing that hasnt changed is the thirst-drink-pee cycle. Florinef seems to reduce this. Any insights you have would be much appreciated.

Hmmm, ive just learned that anaesthetic blocks the AChR receptor. In autoimmune dys there is an AChR receptor antibody which does all the damage-there seems to be a connection. It kind of makes sense to me the body might react to surgery by producing antibodies against the AChR receptor. But why then after a virus would the body attack those same receptor sites? Is it that the postviral autoimmune response produces lots of antibodies and the AChR antibody is just one of them?

Dizzyblonde, re mouth ulcers, i used to get loads until i swapped to herbal toothpaste without sodium lauryl or (laureth) sulphate.

I think you are correct. Ive been researching this myself recently and im 100% convinced.

Im 100 percent convinced my dys is from autoimmune disease. I got mine through pregnancy and c section. Scientists are currently investigating whether there is a role of microchimerism (when fetal cells pass to the mother and stay there for decdes) in autoimmune disease. Prior to pregnancy i did have IBS which i believe in my case has an autoimmne origin. My mother has autoimmne diabetes and my father has asthma and IBS issues. Ive been watching a lot of lectures on the immmune response by dr najeeb on youtube. Very intetesting. I think people who have innate problems with their immune system may go on to result in autoimmunity later in life. This fits with my story: My mother had recently told me that i was always twice as sick for twice as long as my siblings when i was a child. As for treatments, im trying to research that one at the mo.

MomtoGiuliana, Have you seen the stuff on fetal microchimerism? http://www.scientificamerican.com/article.cfm?id=fetal-cells-microchimerism. Im convinced autoimmune disease caused by dys.

This has happened to me too. I take 4 tabs of salt a day plus a drink two gatorades. My salt levels are low and my k levels are normal. I take about 1/2 to 1 tab florinef per day.

Babis, have you found any articles that support the use of IVIG in the treatment of autoimmune disautonomia?

Momto Guiliana. I have been wondering why my bp is so low lying down. I clue came when i started florinef 3 weeks ago. Before that i was constantly thirsty with a dry mouth and was pooing and peeing all day and night. Now with the blood volume enhancement florinef gives me i suddenly am not as thirsty anymore and i have normal saliva levels. The diarrohea and ployurea has also improved. Before i got pregnant i had a very low sodium diet (because i thought it was healthy). Now combine that with hyperhidrosis, and constant vomiting and diarrohea for 3 months of pregnancy and what do you get-hypovolemia. Then top that off with blood loss during c section and mcad response to the anaesthetic (i shook and sweated like i had malaria) and i think that equals hypovolemic shock. I think my body has been trying its hardest and has overcompensated and hence the high standing bp and hr over the last year. The las few monhs though my standing bp has been low (it has gradually lowered over the year). Im currently investigating adrenal burnout as a pontential contributor to this new low bp problem as i have no signs of pooling. I have just been watching some med lectures on youtube which explain the renin angiotensin system. Its no wonder i had massive anxiety as the symp nervous system is triggered by low blood volume. Just a theory. How similar were your post preg symptoms to mine? Oh, i should add that florinef has reduced my lying flushing problem.

I seem to always have low iron too.

For some reason my bp is at it lowest when lying down. After say 10 mins of being in bed i start getting flushing, im no sure what sort of flushing it is though. I think it might be related to low bp. If this happens a lot i can get chest pain. A 24 hr monitor picked up runs of tschycardia lasting about 4 secs if hr 160.

Thanks everyone or posting. Is it like the varicose vein feeling you get when you're in your late pregnancy and your legs ache, feel heavy and it feels nice to put them in cold water?

For those people that have blood pooling in their legs, is it obvious? Is it possible that blood is pooling in my legs but i dont know it? I dont have any discolouration or aching....

Woah, youre gonna look hot in those!