issie Posted April 5, 2011 Report Share Posted April 5, 2011 I'll bump up an article that was recently written on this - maybe you can get something from it. I do believe this has a connection and is part of the key to our problems. Now, I'm also wondering about dopamine levels playing a key role too. Doing research on this one now.Issie Quote Link to comment Share on other sites More sharing options...
ladyt Posted April 7, 2011 Report Share Posted April 7, 2011 ust woundering what is a whater depriving test? and what does it show..?I ust realised that the meds i take to make the nightly visist to the bathroom fewer is a davp type med. it wasnt that many bloodtest i took the the other day. Renin and aldosteron again, and the rest was of somthimg called of the ganiols or somthing. One being growthhormon and my fsh and somthing lke østrogen, but not quiet the same name.So what are my ovulation and growth conection whit reinin and ad..? Quote Link to comment Share on other sites More sharing options...
ramakentesh Posted April 10, 2011 Report Share Posted April 10, 2011 A recent article from vandy confirmed the finding that patients with absolute hypovolumia, paradoxically low renin and aldosterone levels have elevated angiotensin II levels. Reduced catabolism is the likely cause of this. Denervation of the kidneys now seems quite unlikely. This form of POTS could provide the basis for other forms; Perhaps other mechanisms could provide a similar imbalance of neuonal verses endothelial nitric oxide levels in POTS - such as chronic inflammation??There are also patients that simply have low Aldosterone levels. Quote Link to comment Share on other sites More sharing options...
issie Posted April 10, 2011 Report Share Posted April 10, 2011 A recent article from vandy confirmed the finding that patients with absolute hypovolumia, paradoxically low renin and aldosterone levels have elevated angiotensin II levels. Reduced catabolism is the likely cause of this. Denervation of the kidneys now seems quite unlikely. This form of POTS could provide the basis for other forms; Perhaps other mechanisms could provide a similar imbalance of neuonal verses endothelial nitric oxide levels in POTS - such as chronic inflammation??There are also patients that simply have low Aldosterone levels.So, since angiotension is derived from the liver, could liver dysfunction play a key role in this? I've just recently found that I have a lesion on my liver and have always known that my P450 pathways don't detox properly. Now have to find out what the lesion is and how it's contributing to the liver dysfunction. I'm not a drinker or smoker and have ALWAYS been very conscious of eating healthy and trying to be as organic as possible. Don't understand why this dysfunction. Recently, also found that have glutten, dairy and a few other sensitivities. The liver has to process everything. So taking the burden off the liver should help this. If the angiotension II is contributing to this, ACE inhibitors should help. Right? That would explain why added potassium could be a key - because ACE inhibitors increase potassium levels. It would also contribute to increased aldosterone. Wouldn't it? I'm still trying to learn and understand this. Input, would be appreciated. Quote Link to comment Share on other sites More sharing options...
ramakentesh Posted April 10, 2011 Report Share Posted April 10, 2011 Possible I guess but its not what would normally come to mind... Ive had liver issues in the past myself. Quote Link to comment Share on other sites More sharing options...
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