Jump to content

Angiotensin Ii And Its Effect On Water/saline


jangle
 Share

Recommended Posts

Figured I'd make a new thread on this topic.

http://www.ncbi.nlm....pubmed/20228119

Angiotensin ii definitely has some type of mitigatory effect on water consumption associated with some type of protein receptor downregulation. However this doesn't seem to affect saline administration. Now there might be more studies that elucidate more on this topic, I haven't thoroughly searched for them yet, but I believe this explains why saline helps POTS patients and not water + salt (as much) and provides very strong evidence for angiotensin ii.

Link to comment
Share on other sites

  • Replies 58
  • Created
  • Last Reply

Top Posters In This Topic

one of the effects on water is in the kidney breakdown - aldosterone is what comes after angiotension and that is what balances out sodium and water. Allot depends on the balance/levels of aldosterone. Maybe the increased angiotension is to try to stimulate aldosterone production - if that is faulty?????

Link to comment
Share on other sites

Im thinking that would cause the racing heart as well as gastrointestinal and blood flow issues.

Like this makes sense too because like why would spironolactone decrease angiotensin ii? Well spironolactone binds to the aldesterone receptor which would then shut off the angiotensin ii compensatory mechanism thus resulting in lower angiotensin ii.

Link to comment
Share on other sites

But, if there are autoantibody issues spiralactone would increase potassium and this isn't something that the studies have shown that you want to happen. The thought is that the potassium levels are too high with this. There is a fine line between calcium/magnesium and potassium in how it affects the body and in the electrical system output from these minerals. They all affect the heart function and really everything in the body. Get them out of balance and you have some serious problems. Look, some of the heart meds are calcium channel blockers. Others like Lorsartan increase potassium and most of us seem to be low in magnesium and that affects the bodies ability to relax contracted muscles - including the heart. So, we have to know what our balances are in these important minerals and not increase the wrong ones.

Also, if a person - like me with already low aldosterone levels - lowers it even more - you're gonna have some serious problems. Not only am I going to mess my fluid levels up, but also my salt levels up. Plus, people that are taking florinef are lowering their own production of aldosterone - because it's a synthetic version of it. If the function would come back on it's own - I don't know. Or would the body just stop production all together and depend on the administration of it externally? What are we doing to ourselves?

Link to comment
Share on other sites

Did you read the lengthy paper I wrote on this? I had talked with a pharmacist about compounding it for us. It is being used in cats for kidney dysfunction and is compounded to rub into their ears. He said if we could get a doc to write a script he'd do it. I have since learned that he no longer works at that pharmacy - but, don't know if someone else could do it there or not. I listed their telephone number and they would mail it to us and help to tweek it for proper dosage. But, there are dangers involved in using it. Read those papers - I think there may be three of them. Type in renin/aldosterone and it should pull up for you. Testing on rats when using aldosterone and using salt was very, very detrimental. The docs are giving florinef and telling people to up their salt. I don't know - just what I've read and the studies that have been done on rats - you'd think it might kill us too.

He suggested taking a look at cortisol. Because it plays a part in this too.

Link to comment
Share on other sites

Lemons that is true, the parenteral delivery is definitely the difference but I think angiotensin ii is what males the difference occur.

Issie, ya it would not be safe. But now im beginning to think neither would spironolactone. The thing is we have unbalanced steroids that is causing our problems but the body is very sensitive to shifts on steroids so that makes treatment so much more difficult.

Link to comment
Share on other sites

Perhaps something about saline is more sensitive to aldosterone. I.e allowing it to retain more efficiently.

Interesting thought. Not sure about it though. Aldosterone is the hormone that balances the salt and fluid levels. One thing a saline infusion does is up blood volume and also dilutes blood viscosity. So, that may be why the saline infusions help us so much and only last a short time. It helps to thin our blood and thus carries oxygen better to our brains, hearts, limbs etc. and if we're low blood volume and that's increased - we aren't dehydrated any more and we don't have the tendency to pool so bad because there's enough to go around. Our veins don't have to constrict or dilate to accommodate and compensate for the dysfunction - it's temporarily fixed.

Link to comment
Share on other sites

There is still a possibility that aldosterone isn't the primary cause. Drugs like mestinon work well for pots patients despite not influencing the raas directly. Rather the primary defect is the vagus nerve. Perhaps aldosterone secretion is mediated by the parasympathetic nervous system. Therefore a faulty pns would create the environment of low aldosterone. I believe that indeed the faulty pns is due to high angiotensin ii levels and that correcting that should ne the focus of treatment. Maybe it isn't a compensatory mechanism to low aldosterone.

Link to comment
Share on other sites

We have to go back to where the aldosterone comes from - what cycle? Angotension 2 can come from different places, kidney - heart - liver. Aldosterone can be influenced by the kidney and adrenals. I just feel there has to be some sort of connection and I can't figure it out. I've been on this merry-go-round for over a year now and I can't get ANY doctors to address it. Goodness knows I've tried. Maybe now with the uncovering of the possiblity of autoantibodies to ACE2 - this will shine a little more light on it. I was extremely excited when I saw this info and the conection to connective tissue disorders. But, getting doctors to take a look at it - we will see.

Link to comment
Share on other sites

This sounds to me more like a positive feedback system that continues to build upon itself until "papa bear" or the vagus nerve comes in and tells everyone to knock it off. By quickly reducing cardiac output which leads to faint. That is my very scientific and measureable explanation. :) But seriously though, the nervous system and hormonal system building off each other in this manner makes me think positive feedback system.

Link to comment
Share on other sites

No clue Issie. Maybe for those of us who don't faint the vagus nerve is only partially activating which should decrease hr but instead tries to but fails. Triggering more hormone release that overpower the vagus causing faster heartrates. Which sets off the whole shabang. My pots attacks always feel like a tug of war within my body. And the near syncope/ or syncope is the vagus nerve's last pull to win the game.

Link to comment
Share on other sites

Join the conversation

You can post now and register later. If you have an account, sign in now to post with your account.

Guest
Reply to this topic...

×   Pasted as rich text.   Paste as plain text instead

  Only 75 emoji are allowed.

×   Your link has been automatically embedded.   Display as a link instead

×   Your previous content has been restored.   Clear editor

×   You cannot paste images directly. Upload or insert images from URL.

 Share


×
×
  • Create New...