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issie

Renin & Aldesterone - The Article

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RENIN & ALDOSTERONE

What role does this enzyme and hormone play

In this complicated

ISSUE?

By Issie

Some of you may remember the conversations we've had about endocrinology and the role of the adrenals and kidneys. More specifically, the enzyme renin and hormone aldosterone. I've done some research on the possibility of aldosterone being a possible choice for a replacement in balancing the electrolytes of water and salt. (Salt - is a whole other subject. Sea Salt, Himalayan Salt or refined table salt. What's the difference between these chemical compounds and would that make a difference?)

There has been a study done by Dr. Raj showing that people with POTS are shown to be deficient in renin and aldosterone. Renin-Aldosterone Paradox and Perturbed Blood Volume Regulation Underlying Postural Tachycardia Syndrome (Circulation -Journal of the American Heart Association - 2005;111:1574-1582) The conclusion of the study being that the POTS patient has paradoxically unchanged plasma renin activity and low aldosterone given their marked reduction in plasma volume. Also, they have a significant red blood cell volume deficit, which is regulated by the renal hormone erythropoietin. These abnormalities suggest that the kidney may play a role in the path physiology of POTS.

Aldosterone governs sodium transport at several sites in the kidneys. It is triggered by renin, which augments levels of angiotension II and subsequently lead to increased levels of aldosterone. Angiotensin II promotes renal sodium rentition and stimulates the secretion of the mineral corticoid aldosterone - which should balance the fluid volume and salt retention in the body. There are other things that can stimulate aldosterone in addition to the angiogenesis II - potassium and hyponatremia and by the adrenocorticotropic hormone; it is inhibited by dopamine and atrial natriuretic factor (ANF). In this particular study it was thought that electrolyte balance wasn't the issue because sodium and potassium levels were similar with patients with POTS and the control patients. It is thought that impaired vascular function could be part of the issue. There was found to be high norepinephrine levels with higher heart rates and standing with lower aldosterone levels than control subjects. There were no differences between the groups while standing for blood pressure, plasma epinephrine, or plasma renin activity.

So, what do these findings bring up in relationship to POTS and the treatments that we receive? These studies brought up questions for me that I'm trying to find answers for. I found out that salt will lower aldosterone levels. If our aldosterone levels are already low - why would we want to lower it even further. Of course, there is Florinef that is a synthetic form of aldoesterone and causes the kidneys to retain salt. But, that being the case - more salt - less aldosterone. Since aldosterone is what is supposed to help regulate the balance between fluid and salt. Seems to me that aldosterone would be what would be needed to regulate our fluid balance. I know, we all drink or eat allot of salt trying to increase our fluid levels. Because, frankly, we just feel dehydrated all the time - no matter how much we drink. But, is salt the answer, especially a refined salt that has been processed and all the minerals removed? (But that's a whole other story for later.)

I found an article in Dr. Wright's newsletter of May 2006 recommending pharmacies in Canada for aldosterone. (In this newsletter - aldosterone is being used to restore hearing loss. It is also recommended that, if used, your electrolyte levels - potassium, sodium, chloride and bicarbonate be measured at regular intervals along with your aldosterone levels - making sure that they are within a normal physiologic range.) I spoke with a compounding pharmacy in New Mexico; Highland Regent Pharmacy (1-800-243-3777) and aldosterone is available in a transdermal form (at present for animals). And could potentially be tried on humans. When having liver dysfunction it is better to bypass the liver, if possible, when it comes to taking any type of hormones. If it is in a transdermal form, it goes directly into the blood stream and doesn't have to be broken down and transported via the liver. You don't take the chance of not getting the benefit of it.

If you use allot of salt, your aldosterone levels could be low and that could decrease blood pressure and fluid volume. Higher aldosterone levels increase blood pressure and retention of water. It will help release potassium and stimulates uptake of it into cells. When there is low aldosterone levels the potassium feedback is virtually inoperative (according to Wikipedia). So potassium is necessary for proper heart function. The article says that this potassium feedback must take place indirectly from decreased blood flow through the liver due to constriction of capillaries. When the blood flow decreases so does the destruction of aldosterone by liver enzymes. The amount of aldosterone secreted is a direct function of potassium as determined by sensors in the carotid artery. Anxiety also increases aldestrone, as does pain.

Hypoaldosteronism is the name given for low aldosterone. It can cause urinary sodium wasting, leading to volume depletion and hypotension and circulatory insufficiency, high pulse rates/ palpitations, dizziness, lightheadness when you stand, fatigue. It can also cause sweating and a feeling of thirst and craving salt. (Sounds familiar, doesn't it?)

Also, it has been suggested that vasopressin could be one of the issues. I found in Wikipedia that low aldestrone can cause low vasopressin. Then when you add this into the picture you are connecting the adrenals - thyroid - pituitary/hypothalamus. Renin also is supposed to constrict resistance vessels, stimulate release of vasopressin -which in turn, increases fluid retention, stimulate the release of aldosterone which acts on the kidneys to increase sodium and fluid retention, stimulate thirst, facilitates norepinephrine release and inhibits re-uptake by nerve endings. (Articles from Cardiovascular Physiology Concepts by Richard Klabundle, PhD)

Norepinephrine is synthesized from dopamine and released from the adrenal medulla into the blood, and is a neurotransmitter in the central nervous system and sympaththetic nervous system where it is released from the noradrenergic neurons. (Wikipedia) One article from the Journal of Clinical Investigation said that if you have low renin hypertension and you have dopamine infusion it will suppress aldosterone. So if norepinephrine is synthesized from dopamine and we have too much of it (because of a hyperadrenic response) we will have low aldosterone.

According to the paper by Dr. Raj - most POTS patients didn't have low renin. But, did have low aldosterone. Whether the renin isn't signaling for the production of aldosterone or the salt has caused the aldosterone component of the axis to stop producing - who knows? Could it be that because of our high salt intakes we are causing the aldosterone to lower itself even more in order to eliminate the extra salt that we are taking in and we are in fact, compounding our issues. One of our members has used aldosterone, and found it to be ineffective for her. (But, it was in a pill form and I wonder if it was absorbed properly.) She did comment that for the testing to be effective you have to be on a strict salt restrictive diet. That way you can tell if your body is still producing it or if because of salt you are causing your body to suppress it.

What if our bodies are shutting down our renin and aldosterone "because of inflammation". Could it be toxins, bacteria, poor digestion - who knows? It could be auto-immune issues? One article from the Department of Sports Informatics, The Health and Integrative Physiology Laboratory, University of Seoul concluded that acute inflammation is associated with a temporary deterioration in the cardiac autonomic nervous system function in healthy subjects. (So, what is inflammation doing to us?)

One Vanderbilt study done on Mast Cell Activation Disorder and the relationship between hyper POTS showed that the mast cells in the heart produce it's own renin to create Angiotension II. Mast cells in our body have the ability to create renin. The article also mentioned that we don't release sodium through our urine like normal people do. For some reason our bodies retain the sodium. That could explain some of the problem with standing hypertension among hyperadrengic POTS patients. The normal person loses about 14% of their blood plasma after 30 minutes of standing and hyper people lost almost double that amount. Norepinephrine suppresses renin production and it also has effect on the LXRs in our liver. The LXRs in the liver have a connection with glucose metabolism. (Many are having blood sugar related problems.) So, that brings up another question: Which came first in hyperadrengic POTS - high norepinephrine or kidney dysfunction with low renin/aldosterone? So, now, we've also brought the liver into the equation?

Aldosterone will increase fluid retention and arterial pressure. The baroreceptor reflex signals the medulla of the brain stem, RVLM. The medulla, by way of the autonomic nervous system adjusts the mean arterial pressure by altering both the force and speed of the heart's contractions, as well as the total peripheral resistance. The most important arterial baroreceptors are located in the left and right carotid sinus and in the aortic arch. The renin-angiotension system compensates for loss of blood volume in arterial pressure by activating an endogenous vasoconstrictor known as angiotension II. Aldosterone is released from the adrenal cortex in response to angiotension II or high serum potassium levels. Aldosterone stimulates sodium retention and potassium excretion by the kidneys. Since sodium is the main ion that determines the amount of fluid in the blood vessels by osmosis, aldosterone will increase fluid retention and indirectly affect arterial pressure.

Blood viscosity is created when the red cells bunch together and block capillary vessels, the clear fluid of the blood is forced out of the capillary walls and causes tissues to swell. This is called edema. Blood viscosity can be increased by stress. Both types of arthritis are associated with an elevation of plasma viscosity. High blood viscosity leads to a slow down of circulation and reduces oxygenation of the tissues. (Blood Viscosity as a Factor in all Metabolic Diseases; Advanced-supplements.com)

Heart failure leads to the activation of the renin-angiotensin-aldosterone system, which causes increased sodium and water retention by the kidneys. This in turn increases blood volume and contributes to the elevated venous pressures associated with heart failure, which can lead to pulmonary and systemic edema. (Cardiovascular Pharmacology Concepts - Diuretics; Richard Klabunde, PhD) If this becomes an issue then diuretics are used to suppress these levels. It is so important that these levels be monitored because we could create other issues.

High aldosterone levels can also be indicative of Bartter syndrome or from heart or kidney disease or low sodium diets. (Aldosterone: MedlinePlus Medical Encyclopedia) Also, too high aldosterone can promote progression of kidney damage and contribute towards renal injury. High salt up regulates the AT1 receptor; it alters the vessel structure and composition, reduces nitric oxide bioavailability, and increases super-oxide generation. Aldosterone in the presence of even minute elevations in sodium concentration reduces NO generation and increases endothelial cell stiffness. Aldosterone is one of the most neglected aspects of renal disease.

Excessive concentrations of aldosterone are not necessary to cause serious target organ damage. Activation of the mineral corticoid receptor by cortical in states of malfunction of the cortical degrading enzyme are factors for the adverse effects of normal aldosterone concentrations, somewhat misleadingly called relative aldosterone excess. If maintained on a low salt diet, rats do not develop high BP or vascular damage. The effect of sodium caused the vessels to swell and stiffen. In the presence of aldosterone, the stiffness increased within minutes when the sodium concentration was increased once a threshold of 135 mmol/L was transgressed.. So not only is sodium balance important, but so is sodium concentration. So, it is important to lower salt intake when you are treating patients with kidney disease. (How Little Aldosterone is able to Raise Blood Pressure? Eberhard Ritz; Clinical Journal of the American Society of Nephrology)

There is also a connection between hyperglycemia (diabetes) and renin release. Ionized calcium was known to be involved in the control of renin release, and calcium-sensing receptors as well as vitamin D receptors are present on juxtaglomerular cells and modulate renin release. (Clinical Journal of the American Society of Nephrology).

Lower than normal aldosterone levels may indicate: Addisons disease, hyporeninemic hypo aldosteronism, or high sodium intake. Of interest, there are medicines that can affect the aldosterone levels:

ACE inhibitors, Calcium channel blockers, diuretics, heparin, lithium, non steroidal anti-inflammatory drugs, propranolol. (Aldosterone: MedlinePlus Medical Encyclopedia)

Potassium levels are the most sensitive stimulator of aldosterone. Aldosterone is responsible for the reabsorption of about 2% of filtered sodium in the kidneys, which is nearly equal to the entire sodium content in human blood under normal GFR. The slope of the response of aldosterone to serum potassium is almost independent of sodium intake. Aldosterone is much increased at low sodium intakes, but the rate of increase of plasma aldosterone as potassium rises in the serum is not much lower at high sodium intakes than it is at low. Thus, the potassium is strongly regulated at all sodium intakes by aldosterone when the supply of potassium is adequate. (Wikipedia)

So, in conclusion - we've discovered that this is a very complex, multi organ involved syndrome. You need to know about nephrology (kidneys), GI (liver), cardio (heart and blood vessel structure and function), endocrinology (hormone and enzyme balance, thyroid, pituitary, hypothalamus, adrenal), allergist (allergies related to mast cells), auto-immune issues. And the list could possibly continue on …. And on….. And on.

So, should we or shouldn't we continue on with the florinef and heavy salt loading? Would a possible trial or study on using transdermal aldosterone be helpful to us? Some medicines lower aldosterone too (like propranalol; MedlinePlus Medical Encyclopedia). Are we compounding our issues with these meds? Does anyone really have the answers? Could we all participate in a little out of the box thinking and analyze what we've been doing, is it working? If it's not working, what other possibilities are there? We know how we feel. We need our doctors to participate in our journey and try new things and come up with other alternatives. But, because it's our world - lets embrace it and come up with solutions. I'll be looking for you - "Out of the Box" thinkers. PM me and we will get some of your thoughts out there. Who knows - maybe we will come up with "THE" Answers.

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I am going to print this so I can review it better - my eyes don't focus on the screen in the afternoons for some reason. I am health info fanatic (I used to eat, sleep, live nursing), but I have not examined any of this in relation to POTS...seems like an interesting read and some areas worth exploring. Thanks for posting,

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Issie-

So glad we finally get to see your article!!! Forgive me, in advance- I'm going to bombard you with questions :blink:

In low flow POTS, apparently very high levels of angiotensin II are present (Vandy's latest research.) Additionally, angiotensin II has been implicated as a cause of mast cell activation. It also seems to be implicated in endothelial inflammation, creating a profibriotic environment affecting both cardiac & renal function. All of this describes me :rolleyes:: low flow, MCAD & a scarred up heart causing the diastolic dysfunction and most likely reynauds as well.

In your article, I didn't understand how blood viscosity was affected by aldosterone... That's another of my issues :blink: Help me understand that, Issie.

If I understand your article, aldosterone RAISES angiotensin II- which is already present in very high levels in my body??? So, it wouldn't be an appropriate therapy for me= would it? :( . Can you see why I'm so excited about Lorsartan that inhibits angiotensin II? :D

So maybe a higher salt diet would benefit me- except THAT is also implicated as a causal factor in diastolic dysfunction- so confusing! It's so hard to separate what's causing what...

I'm also guessing that an angiotensin II test to check levels must not be readily available..

I think you're on to something BUT it may not apply to ALL of us. I was also concerned to hear that the transdermal aldosterone patch had only been used on animals...

Thank you for sharing & for all of your hard work. I'm convinced that it's patients like us who will solve our own issues.

Julie

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thank you very much. need time to read and re-read---and read again! best, cordelia

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Mack's Mom,

When you mention all the problems and connections , it sounds like "who's on first..." :P We can all just give a collective *sigh* on how complicated this all is! It is ALL so connected, but jumble them all up, and we will wait to see which of the issues seems to keep "making noise". In other words, as we all keep hashing this out, something is going to begin to turn up more and more with our labs or odd symptoms that will possibly make sense--I hope.

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Julie,

You're right. I don't think that it would be good for me - hyper POTS. But, for those with the low bp's (the ones that Florineff seems to help) the aldesterone probably would be good. But, you have to have a doctor to prescribe it and to keep a close watch on levels because as mentioned in the article - you don't want it too high because there would be bad consequences. Also, if you used it you would NOT (NOT) increase your salt. The aldesterone would be helping the fluid balance and the salt wouldn't be necessary and could be VERY determinatal. The pharmicist that I talked to about our POTS and my ideas - said that he would be willing to compound for humans if we could find a doctor willing to RX and moniter us. It would be a cream that would be applied transdermally. (Easy to adjust dosages to find optimal amounts.) Aldesterone levels can be checked with a simple blood test. So, it's not hard to figure out where your levels are. Mine was low and my noriephi was high. (Same response as the study - the high noriepi levels causes the aldesterone levels to be low.)

With the new study from Vandi - the med is a form of potassium. That's why my comment on - why not just take potassium and see if it balances things out. It would be a simple test that you could do. I believe that the balance between minerals is cruical. You get one out of balance and you could throw them all off. Too much sodium (raises bp) and too much magnesium (lowers bp). Opposite ends of the spectrum. Why don't we have more mineral test done and see if we're out of balance in our minerals? Our bodies make vitamins, but does not make minerals. If we don't eat healthy or have digestive issues - we may be deficient in minerals.

Since aldesterone affects the balance of fluid in the body. That's how it affects blood viscosity. If you're fluid levels are too low because the balance isn't balanced (possibly because of) aldesterone. Wal-la- lack of fluid = concentrated blood. Lack of oxygen because the blood doesn't flow properly and it doesn't carry oxygen properly.

I'm learning these things and drawing my own conclusions - if my conclusions are wrong - someone please tell me. But, from a logical deduction - I think I'm on to something. I truly believe that all the doctors can't be wrong when they show you how bad TOO MUCH salt can be for us. As I mentioned before - it can cause congestive heart failure and renal failure. Two things that are already affected by us having POTS. Are we compounding the issues by adding a whole lot of salt to this mixture. Lowering aldesterone which is what is supposed to balance fluid levels and balance blood pressures. Not to mention that the med used Florineff is a synthetic form of aldesterone which in turn will cause the body to stop producing it's own and rely on the med. This could possibly happen with the transdermal form too - but it seems that it would be a more natural way to suppliment than a synthetic form. At least if your liver doesn't have to process it - it wouldn't affect that part of your body so adversly. And I think that probably potassium wouldn't hurt us to supplement - maybe a full spectrum multi mineral, so that things stay in balance. (Of course, you have to know that some mineral won't create a problem for you. ie. Wilson's Disease that accumulates too much copper or Hemocromatosis that accumulates too much iron.)

As for your rynaulds, that is considered an autoimmune issue and autoimmune issues do play into POTS. My IGG was very low. I have vitiligo - which can be caused by autoimmune issues or adrenal issues - both can be connected to POTS.

As for salt. I feel we do need salt - but not HIGH SALT LOADING. I know I feel better with salt and I do crave it. But, I don't salt load or use more than the normal amount on my food. If I feel dehydrated - I'll slowly sip a G2 and use water in between the sips. A doc told us to do this for the cells to have time to uptake the salt and potassium (for electrolyte balance). Possibly, the potassium is just as important as the salt and that's why we feel better with an electrolyte mixture. But, since I feel that minerals are SOOOO important - I feel, that only salt that isn't refined and broken down should be used. (Sea Salt or Hymilaian Salt - that has all the minerals still in it and is not refined.) That was going to be my next research project and when this article got shot down - it kinda killed the research in me. I put a whole lot of time and energy and thinking into this article and felt it was so important to be considered and - until now - thought no one would benefit from what I felt could be part of the answer. So, maybe I'll dig out all the stuff I had started researching in regard to salt and the different forms and why it's important to use the unrefined forms of it.

Hoping for feedback on this and hoping that it stirs up some interest and possibly some research from those that CAN make a difference.

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Thanks for the clarifications, Issie. I LIKE the way you think & question status quo. Keep up the great work!

Julie

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Mack's Mom is right - in most cases renin stays inappropriately low in the face of orthostatic challenge and absolute hypovolumia because in this subset of hyperadrenegic patients, angiotensin II levels are inappropriately high due to decreased catabolism from faulty ACE activity.

Angiotensin reduces the bioavailability of neuronal nitric oxide which is a major marker for the nitrergic nerves of the parasympathetic system. reduced NO also potentiates norepinephrine and also increases overall inflammation.

Patients with increased angiotensin II would have low flow or hyperadrenergic POTs with low blood volume and supine vasoconstriction, increased inflammatory markers, reduced cutaneous blood flow and potentially mast cell activity.

By the way the Vandy study only confirmed Julian Stewart's earlier work.

The good news is that if you have this form of POTS its gonna be easier than most to treat affectively.

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Rama-

Good to see you back- we missed you. Question: Can angiotensin II levels be checked? If so, is there any trick to getting the blood draw- does the patient have to be upright vs. sitting, etc. And, what sort of doctor would do this test?

Thanks for your help-

Julie

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Julie,

Quest Diagnostics can test for Angiotensin II; I think it's a blood draw with some tricky requirements on the part of the lab. Dan's neurologist wouldn't order the test :angry: so his pediatrician ordered it but ordered the wrong test :( so we never figured out what Dan's Antiotensin II level actually was prior to starting the Losartan.

I also get the sense that the test may not be a particularly reliable measurement (anyone can correct me if I'm wrong on that) so I wouldn't necessarily use the Angiotensin II level as a determining factor of whether to try a treatment or not.

Lenna

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I know I'm hyper POTS - I do have autoimmune issues - My CRP is also normal. I never understand how my CRP is normal when my body feels like it's in a constant state of pain and is one BIG OWE-EY. I never feel hydrated - no matter how much I drink and salt was not good for me - nor any of the POTS meds I've tried. So, if this type is supposed to be easy to treat - no ones figured that out YET.

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Julie,

Quest Diagnostics can test for Angiotensin II; I think it's a blood draw with some tricky requirements on the part of the lab. Dan's neurologist wouldn't order the test :angry: so his pediatrician ordered it but ordered the wrong test :( so we never figured out what Dan's Antiotensin II level actually was prior to starting the Losartan.

I also get the sense that the test may not be a particularly reliable measurement (anyone can correct me if I'm wrong on that) so I wouldn't necessarily use the Angiotensin II level as a determining factor of whether to try a treatment or not.

Lenna

How is he doing since he started the new meds? Has it made a difference?

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"There has been a study done by Dr. Raj showing that people with POTS are shown to be deficient in renin and aldosterone. Renin-Aldosterone Paradox and Perturbed Blood Volume Regulation Underlying Postural Tachycardia Syndrome (Circulation -Journal of the American Heart Association - 2005;111:1574-1582) The conclusion of the study being that the POTS patient has paradoxically unchanged plasma renin activity and low aldosterone given their marked reduction in plasma volume. Also, they have a significant red blood cell volume deficit, which is regulated by the renal hormone erythropoietin. These abnormalities suggest that the kidney may play a role in the path physiology of POTS"

It is interesting to me how everyone could be suffering from a lot of the same symptoms, but have different causes. This article from Dr. Raj really struck home for us. My daughter's problems are similar in manifestation to everyone here, except she has more NMH than POTS. Because her issues stemmed from head trauma, she has low everything: inappropriately average renin, non-existant aldosterone, low/avg norepinephrine lying down with zero response on standing, low cortisol and interestingly no cortisol response (elevation) to stress. She had a formal blood volume test and falls right in with the people from the above study - 21% blood volume deficit, 17% plasma volume deficit and 29% red blood cell deficit.

When she first got sick after the concussion, her blood was so thick that it would take a tech forever to draw it. She was often dizzy and unstable for days after a blood draw. I guess she is hypoadrenergic all around. Instead of a hyper response, what we have going is no response to upright posture, stress, anything.

For her, florinef (aldosterone) works wonderfully. When she had to go off it to see Dr. Stewart, and we only came off for 4 days for the blood volume test, she felt terrible. Makes me wonder if her dose shouldn't be higher. I will say from personal experience with her now, the kidneys absolutely play a role and are affected - at least for her. Her hematocrit is low and her red blood cell count is also low. She has very little peripheral resistance throughout her body and her blood vessels and capillaries don't constrict with upright posture. They can still, but she has to have a very strong emotion of some sort to drive it - anger, fear, excitement. Its like her on/off switch is broken and only works for half an hour or so on its own if you "hit it" with that strong emotion. Her blood vessels constantly "leak" fluid because they don't have anything that sends the norepinephrine to constrict, so she gets edema - frequently.

She was started on procrit (erythropoietin) in December as well as Octreotide. On top of the midodrine, florinef, dextroamphetamine, etc that she was already on. All of the latter work for her but the procrit has been one of the best for giving her a little more energy and the octreotide has been amazing at helping to somewhat control the fluid leakage in her midsection. Its not a cure, but it has definitely helped. So now she has a small "bucket", as i tell her, of the things her body needs to respond to the body's stress, but unlike folks who aren't sick, her bucket doesn't expand when needed. It has only what the drugs give her. So, on days that she studies a lot, or is up late, she uses up the bucket (and we've definitely learned that studying uses up a lot of that bucket) and she swells more and her body and brain work badly the next day. Even things like spending too much time on a computer, really depletes her. So, we are grateful for the slightly bigger bucket from the procrit. We wish it had a response switch but its certainly a moderate improvement over two years ago.......Just thought i'd share in case anyone else has similar issues since we have learned (and are learning) so much.

Kate

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As explained previously it is now prettymuch accepted that nearly all hypovolumic POTS patients have elevated angiotensin II levels resulting in paradoxical renin responses to orthostatic stress.

So Raj's most recent work confirmed this finding. Angiotensin II and faulty ACE 2 activity is the culprit in hypovolumia.

NO levels are very hard to measure and we are talking neuronal nitric oxide and not endothelial.

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As explained previously it is now prettymuch accepted that nearly all hypovolumic POTS patients have elevated angiotensin II levels resulting in paradoxical renin responses to orthostatic stress.

So Raj's most recent work confirmed this finding. Angiotensin II and faulty ACE 2 activity is the culprit in hypovolumia.

NO levels are very hard to measure and we are talking neuronal nitric oxide and not endothelial.

What is the standard form of treatment for this, if this is the case? Is there some way to get your body to reverse this response? I'd really like to do things with natural supplements/or foods rather than chemical medicines.

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How is he doing since he started the new meds? Has it made a difference?

He had been doing quite a bit better, but then we started playing around with the dose and he crashed. He's back on his original dose now, but Losartan takes a while to have an effect, so it may be a week or two before he gets back to where he was. IF he gets back to where he was...

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He had been doing quite a bit better, but then we started playing around with the dose and he crashed. He's back on his original dose now, but Losartan takes a while to have an effect, so it may be a week or two before he gets back to where he was. IF he gets back to where he was...

I HATE to hear that. :( I have been very curious to hear about Danny's progress. So when you raised the dose from the initial starting point, he crashed? So sorry, Lenna. I pray he will return to his previous improved level of functioning.

Hugs-

Julie

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Hey Julie...

Here's what happened. He was functioning a notch better than his POTSY normal when he was taking 25 mg. of Losartan in the morning. In the hopes of getting to 2 notches better, he increased the dose by 1/2 pill (12.5 mg.). The other change he made was to take that half pill at bedtime in the hope that he might have better quality sleep and wake up feeling better. Unfortunately, that is not how his body responded. After 2 weeks of feeling crappy, he cut the morning dose back to a 1/2 pill, so he was taking 1/2 pill 2x day. Again, he spent the next 10 days feeling terrible. So now he's back on the original dose of 1 pill only - 25 mg. - in the morning. It's been about 5 days and he hasn't felt well at all, but I'm hoping that things improve over the next week. The problem is that there is no one to advise us. Losartan is such new territory. But I'll keep you posted on how things go.

Lenna

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Hey Julie...

Here's what happened. He was functioning a notch better than his POTSY normal when he was taking 25 mg. of Losartan in the morning. In the hopes of getting to 2 notches better, he increased the dose by 1/2 pill (12.5 mg.). The other change he made was to take that half pill at bedtime in the hope that he might have better quality sleep and wake up feeling better. Unfortunately, that is not how his body responded. After 2 weeks of feeling crappy, he cut the morning dose back to a 1/2 pill, so he was taking 1/2 pill 2x day. Again, he spent the next 10 days feeling terrible. So now he's back on the original dose of 1 pill only - 25 mg. - in the morning. It's been about 5 days and he hasn't felt well at all, but I'm hoping that things improve over the next week. The problem is that there is no one to advise us. Losartan is such new territory. But I'll keep you posted on how things go.

Lenna

Thanks for those details. You know I am praying for Danny to regain his lost ground. It's so hard on our kids when they worsen- the world still expects so much of them.

I just wanted to add that I KNOW exactly what you mean about there being no one to oversee his trial. I am collecting proof (medical studies) that this is the best med for me to try next and plan to "sell" it to my rheumy. Then, Ill just follow Danny's lead with dosing... Frustrating.

Which doctor recommended this med for Danny? Could s/he help with dosing issues, setbacks, etc. Forgive my curiosity, but how did you KNOW that Danny was low-flow and might benefit from this therapy? From what I've read it's rare for males to fall into this category. That being said, I suspect Mack is low-flow too :rolleyes: .

Hugs & prayers to you both-

Julie

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Thanks for those details. You know I am praying for Danny to regain his lost ground. It's so hard on our kids when they worsen- the world still expects so much of them.

I just wanted to add that I KNOW exactly what you mean about there being no one to oversee his trial. I am collecting proof (medical studies) that this is the best med for me to try next and plan to "sell" it to my rheumy. Then, Ill just follow Danny's lead with dosing... Frustrating.

Which doctor recommended this med for Danny? Could s/he help with dosing issues, setbacks, etc. Forgive my curiosity, but how did you KNOW that Danny was low-flow and might benefit from this therapy? From what I've read it's rare for males to fall into this category. That being said, I suspect Mack is low-flow too :rolleyes: .

Hugs & prayers to you both-

Julie

Julie, I sent you a PM. It's a long story...

Lenna

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Thanx issie... :D

really greatfull...

I have to read it and reread it over and over again, and might try the google translater also. The translaiton is not perfect, but migth help. Being dyslexix dosnt really help either. But after years of reading sort of easy to read english lit, i gett a litle more than i used to.

I miss my brain, not that is was that great in the beginning, but still.. But i gess i have to keep trying to understand. Even if i really dont at all. Somthing has to stick eventually :P being stubborn i gess is not all bad ;)

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I think you're doing really well with English if you get anything out of this. For us that speak English it's like a second language. It's hard for anyone to understand and very deep too. Glad you enjoyed it.

Just as a side note - and will start another post. Just ran across an article showing that people with heart failure - usually have higher levels of aldosterone and lower levels of DHEA. Wondering if the high use of florinef (synthetic aldosterone) is imbalancing the DHEA levels even more. I'm thinking that aldosterone is a key player here, but wondering if having too high levels either from an outside source (meds) or just naturally - plays a part in this. I'll start another thread to consider this. Wonder if people are having their DHEA levels checked, who are on florinef?

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sounds like u are deep in detectiv work issie :D .. And that u understand this a hole lot more than i do..

All i gett is my gutt feeling that all this hormon stuff is the key for many of us...

i whant to start on florinef, but have to gett an apointment whit a cardio to do so...

Hmm i have to find out what DHEA is and then if i mght have been tested for it. Since they never have tested my renin and adosterol levels before, they propl havnt..

keep up the dectecive work B) ... And i will keep trying to gett somthing to stick....

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