Le Blanc Rodentia - Perindopril test
 

This White Rat has succeeded in persuading his GP to switch his hypertension medication to perindopril. Perindopril is an ACE inhibitor but is a little special. For one thing, it is one of only two that penetrate the BBB. For another it seems to increase dopamine levels and improve symptoms rather dramatically as the reports below indicate. I took the first one yesterday and another today and I do think that I see a change. I am going to experiment with time of day first. Assuming that my kidney function holds up (the only serious potential side effect) I will keep you all in the loop.

-------------------

1. Aust N Z J Med. 2000 Feb;30(1):48-53.

The angiotensin converting enzyme (ACE) inhibitor, perindopril, modifies the
clinical features of Parkinson's disease.

Reardon KA, Mendelsohn FA, Chai SY, Horne MK.

Neurosciences Department, Monash Medical Centre, Melbourne, Vic.

BACKGROUND: Animal studies have demonstrated an interaction within the striatum
between the angiotensin and dopaminergic systems. In rats, the angiotensin
converting enzyme (ACE) inhibitor, perindopril, crosses the blood brain barrier
and increases striatal dopamine synthesis and release. In humans, angiotensin
type 1 receptors have been found on dopaminergic neurons in the substantia nigra
and striatum. In Parkinson's disease, there is a marked reduction of these
receptors associated with the nigrostriatal dopaminergic neuron loss.
AIMS: We performed a double blind placebo controlled crossover pilot study in
seven patients to investigate the effect of the ACE inhibitor, perindopril on the
clinical features of moderately severe Parkinson's disease.
RESULTS: After a four week treatment period with perindopril, patients had a
faster onset in their motor response to L-dopa and a reduction in 'on phase' peak
dyskinesia, p=0.021 and p=0.014 respectively. Patients also reported more 'on'
periods during their waking day in their movement diary, p=0.007. Perindopril was
well tolerated without any significant postural hypotension or renal dysfunction.
CONCLUSIONS: These results suggest that ACE inhibitors such as perindopril may
have a place in the management of motor fluctuations and dyskinesia in
Parkinson's disease and justify further study.


PMID: 10800878 [PubMed - indexed for MEDLINE]

Week One
 

For the first time today I caught myself thinking, "Damn! This stuff may actually be working!" I quickly stifled myself lest the Gods of Placebo be aroused but thought it time to report.

The first days were tough. Perindopril makes my symptoms worse for a couple of hours and I feel like crap, too. This is not a drug for taking when you need a boost. Things were not helped any by my GP's prescription of 8 mg daily when the manufacturer says start at 4 mg and go up to 8 mg after a month to get used to it. So I was a bit disappointed at first. But I twinked and fiddled and have found that 4 mg at bedtime avoids the problems.

I have fixed the problems that I created, but have I gained anything yet? Until today my answer would have had to have been, "Welllll, maybe." After all, it had barely been a week. While I had a feeling of favorable change, it was pretty vague and might have a certain amount of wishful thinking. And just last Friday, a mere three days ago, I had rushed home at mid-day just steps ahead of a couple of hours of "offtime". So I was a little paranoid and was going to be cautious.

Honestly, that was my intent. I don't know how I ended up at WallyWorld. Not just at it, but all over it for over an hour followed by a stop at a grocery store on the way home. Folks, I have pretty much been home bound for the last couple of weeks due to some problems with entacapone. Going up to the mail box in this heat had been a big deal. But today I surprised myself and conquered Mt. WalMart.

True, I did need an hour of recovery when I got home. But it beat collapsing in the floor with the pooches like I would have done a week ago. And tomorrow may be worse. But it may not. And it is true that I have a little dyskinesia. But I am trying to reproduce a bloomin' *40%* increase in the dopamine levels in my brain in one month's time! A little Dk is a sign that it may be happening, so I will start whittling the sinemet and requip down. Already have.

And so, onward - through the fog....

Serious business
 

I joke around a bit, but perindopril is turning out to be a very serious matter. I am increasingly pleased with it. Things seem to be improving across the board. Off times have been limited to about an hour at mid-day and even that is dwindling. I no longer feel house bound and am out and about even with this blasted heat. It is an old drug, cheap, and well tested for hypertension. Any GP around can prescribe it if your neuro wont.

Gee Mr. White Rat,

I tend to joke around a bit too, but you continue to amaze me with your knowledge of whatever this Parkinsendocrine thing is that we suffer with. Good luck to you in your pursuit of answers Reverett un do trois.

sincerely jb49

Thank you jb49 and glad to see you here. The white rat thing is an old joke originally poking fun at our poverty (We can afford only one rat. Call me "squeaky" for short.):D

Reverett123,

You amaze me with the knowledge you have of this disease. You sound like a doctor and really appreciate the way you keep us informed.

I just want to ask, so far has there been any side effects? If so, what have there been?

Please keep us informed as often as you can, I for one need the assurance that there's always some kind of hope for anyone caught in this dreadful disease.

thank you
keep up the good fight
cp

no side effects yet
 

Other than the problems noted above that led me to bedtime as when to take it, I haven't noticed anything. Also the small study near the beginning of this thread doesn't mention any. My background is a little odd. I studied PD for three years alongside a French surgeon named Anne Frobert, herself a PWP.

Yesterday was the best in a very long time. No "off" time at all until nearly bedtime!

So why should it work?
 

Like everything else about this dratted disease, nobody knows, so a guess will have to do. Angiotensin has strong pro-inflammatory action and the perindopril counters that. Since it is one of the few things able to pass the BBB, it is able to go deep into the brain and calm things down. That makes since to me but it is still a guess.

Yesterday (Sat 7/31) was another good day. No "off"time until evening when I cut short the medication day to see what would happen. Even that was improved. Most interestingly, I experienced a moment of, for lack of a better term, "fluidity" when my muscles worked smoothly as I turned my body. This is hard to explain, but it was as though my body realized that the turn was going to leave me open for a fall, belatedly began to brace for it, and was surprised when it did not materialize.

Another change- My medication cycle has an unfortunate feature. As sinemet comes on I must urinate. But this occurs before motor function returns. The result is that I make regular use of a chairside urinal. Or at least I did until yesterday when I realized that the whole day had passed with the urinal unused.

Found this review of the small study that started this thread:

"esults

Six subjects completed the study - one withdrew with nausea, malaise, and increasing 'off' periods while taking perindopril. After 4 weeks on the ACE inhibitor, 5 of the 6 had a significant increase in the area over the curve for their Webster scores, indicating an increased motor response to their standardized dose of L-dopa. There was a faster onset, and a reduction in 'on' phase peak dyskinesia.

The UPDRS II scores showed that perindopril was associated with improved functional ability in 'off' phases. The patient diaries revealed a modest but significant increase in 'on' periods during ACE inhibitor treatment, which was maximal in the 3rd and 4th weeks on the drug.

While peak dyskinesia scores were reduced, four of six patients had an increase in dyskinesia during the waking day with perindopril. This was probably a reflection of their increased total 'on' times.

There were no perindopril-related adverse effects on blood pressure, postural hypotension, or renal function.

Comment

This study confirmed the concept that an ACE inhibitor can improve the motor response to L-dopa in patients with Parkinson's disease. The drug also increased the proportion of the day spent in the 'on' state, as well as showing an improvement in the functional disability scale used.

Most effective agents in Parkinson's disease induce dyskinesia; perindopril, on the other hand, produced a greater amplitude of motor response to L-dopa with a reduction in peak dyskinesia, i.e. it seems to have an effect beyond simply increasing dopamine release.

The authors of the study point out that the benefits of perindopril were "modest, and not of the magnitude of L-dopa itself". However, the dose was relatively small, and treatment duration was short. As tolerance as good, there is every reason to conduct further studies with higher doses, for longer treatment periods.

Trandolopril, spiropril and perindopril are ACE inhibitors that can penetrate the blood-brain barrier, while enalapril cannot."

patent
 

Patents are mind-numbing, but if anyone wants to interpret for the rest of us

Neurogenesis by modulating angiotensin
United States Patent 7858611

more baseline data
 

A basic exercise- How long can one stand on one foot? Best out of five attempts. Test during maximum "on" period for the day.

Two days ago I got zero on each foot.
Today I got five on my right foot and six on my left.

This afternoon it is seven seconds on the right and nine seconds on the left. Also, I skipped a pill at 2:00 with seeming impunity.

It has been rughly a month now and I am quite encouraged with the perindopril. I am also a little hacked off that I wasn't taking it from the day of diagnosis.

I am still a work in progress. My days are much more stable with very little OFF time. I have ditched the ropinerol again and am running on 8x sinemet cr, two hours apart, and continue to lower that. I turn over in bed with little trouble. When I waken to Nature's call in the night (roughly every two hours), my legs are much stronger. There is more muscle mass there, too, and the atrophy has been reversed.

The biggest problem is dyskinesia. I am not too surprised since the earlier study indicated dopamine increase.

I pronounce this to be "Good Stuff"!

RLSmi, thank you. It is nice to know someone is watching. Plus I have a question for you in particular. As I recall, you have been taking low dose dextromethorphan at bedtime for several years. My question is, "What prompted you to select that timing?"

I have settled on a similar schedule for the practical reason that for a couple of hours after taking perindopril my symptoms actually worsen. Taking it at bedtime gets around that. But I have to consider the possibility that other factors similar to those that guide you are at work.

Yesterday I experienced zero time either off or frozen. Almost no dyskinesia as well.

Rick; I began using DM as an OTC substitute for low-dose naltrexone. The basis for taking it at bedtime is the theory put forth by Ian Zagon at Penn State that the cells that produce endorphins and their receptors do so in the middle of the night. The brief "spike" of the drug a couple of hours before then apparently stimulates greater production of the endorphins and receptors, with the effect of enhancing regulatory control of the innate immune system (macrophages and microglial cells). Check references in the LDN web page on Zagon's earlier work for more detail.

On the other hand, Hong's work on suppression of inflammation by these morphinan drugs suggests that a specific enzyme in the microglia responsible for producing superoxide and hydrogen peroxide is the target for the drugs, with the enzyme action being inhibited by extremely low concentrations of not only these morphinans but endorphins themselves!

I can't figure out exactly how the two different explanations might be connected, but the bottom line is that low-dose DM or naltrexone seem to work with some people.

This is probably way more information than you wanted this morning, but I seem to have a hard time stopping once I get rolling on this subject!
Robert

Rick; I failed in my first reply to address your question about the possible connection between your apparent better response to perindopril taken at bedtime and DM taken at bedtime. I have no clue as to what the connection might be. Of course there are myriad known diurnal changes in the endocrine system(s), any one (or more) of which could be affected.
Is perindopril an ACE inhibitor (similar to lisinopril)? My impression was that perindopril's antihypertensive effect has to do with calcium ion regulation.
Robert

It is not so much that there is a better response as it is an initial negative effect lasting a couple of hours. I haven't run across the calcium link. One suggested explanation was that angiotensin2 is a pro-inflammatory cytokine and that its suppression is thus beneficial.

A couple of interesting points- There are only two ACEIs that can pass the BBB, captopril and perindopril.

Research indicates that blueberries have something going for them vis-a-vis PD. Blueberries are also a natural ACEI.

And check this one out-

1. J Neurochem. 1999 Jul;73(1):214-9.

Effect of chronic angiotensin-converting enzyme inhibition on striatal dopamine
content in the MPTP-treated mouse.

Jenkins TA, Wong JY, Howells DW, Mendelsohn FA, Chai SY.

Howard Florey Institute of Experimental Physiology and Medicine, University of
Melbourne, Parkville, Victoria, Australia.

We have previously shown that chronic treatment with the angiotensin-converting
enzyme inhibitor perindopril increased striatal dopamine levels by 2.5-fold in
normal Sprague-Dawley rats, possibly via modulation of the striatal opioid or
tachykinin levels. In the present study, we investigated if this effect of
perindopril persists in an animal model of Parkinson's disease, the
1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated mouse. C57BL/6 mice
were treated with the neurotoxin (30 mg/kg/day intraperitoneally) for 4 days and
then left for 3 weeks to allow the degeneration of striatal dopaminergic
terminals. At this time, the mice exhibited a 40% decrease in striatal dopamine
content and an accompanying 46% increase in dopamine D2 receptor levels compared
with control untreated mice. The dopamine content returned to control levels, and
the increase in dopamine D2 receptor levels was attenuated in mice treated with
perindopril (5 mg/kg/day orally for 7 days) 2 weeks after the last dose of MPTP.
When the angiotensin-converting enzyme inhibitor was administered (5 mg/kg/day
for 7 days) immediately after the cessation of the MPTP treatment, there was no
reversal of the effect of the neurotoxin in decreasing striatal dopamine content.
Our results demonstrate that perindopril is an effective agent in increasing
striatal dopamine content in an animal model of Parkinson's disease.


PMID: 10386973 [PubMed - indexed for MEDLINE]

Went shopping this morning. As I came out into the bright sunshine, I was briefly blinded and missed the curb. Went careening toward a 3-point landing onto my nose. But my feet managed to catch up with the rest of me and avert disaster. A similar mishap back in the winter cost me seven stitches in the forehead.

Wonder drug?
 

Glad to hear your feet caught up with you before you face planted. Ouch!

Perindopril sounds like a sure thing. I guess it faces a lot more research and studies, though.
I wish I had high blood pressure instead of LBL. I'll never be able to benefit from this drug. Last night my blood pressure was 97/59 after becoming short of breath from doing laundry. Heart rate was 75, but in the past had stayed around 60.
The good news is that many PWP may be able to live better lives with this drug.

Thanks for sharing your experience with it, Reverett.

Tonya

still looking good
 

The last few days have featured a good bit of dyskinesia. But yesterday I started taking half pills on the same time frame and am seeing big improvement. Probably a rocky road ahead as I walk a tightrope between quiver and catatonic.

But isn't that what I should expect if neurotransmitters are ramping up? I mean 2.5x is an impressive number.

There are other ACEs that cross the BBB:

http://www.medscape.com/viewarticle/556014

I am following this thread with interest. I switched to lisinopril a few years ago from Vasotec for this neuroprotective reason. Altace is to be avoided if possible because it has some toxic long term effects. This drug may cause liver problems and should not be used by patients with pre-existing liver damage.

Lisinopril on the other hand is not appreciably liver metabolized and is excreted for the most part whole by the kidneys.

Today was another of those where I suddenly got a flash of "Hey! I AM doing better than I would expect! Twice this afternoon I cut a sinemet CR in two. Not bad.

Another change noted last night. A thunderstorm knocked out our power, wife was out for the evening, and it looked like peanut butter in the dark for supper. I threw caution to the winds, drove to a local restaurant in the dark, ate and returned home. In the last five years I could count the times that I have driven in the dark and alone on one hand.

It was a dark and stormy night...
 

Mazel tov! These little triumphs should serve to highlight just how much we lose to this horrid disease. It sure feels great to know that life's simple pleasures are not entirely lost to us forever. Savor every moment.

Rick could you please give us an update on your med regime now vs. before starting this drug. Also would you be willing to share BP levels pre and post. Like a brief data summary?

How many mg are you taking currently? I so want to try this but don't have chronic high blood pressure. I take it you no longer need propanalol and have stopped Amantadine?

Thanks! I am thinking of talking with my neuro about this and want some serious real world ammo.

You might be a poor white rat but you are an intrepid rat. :D

Laura

Laura-
I am currently taking one 100/10 generic LD/CD upon awakening (from 6:00 to 7:00 AM). Then it is one 200/50 generic CR of same every two hours starting with 8:00 AM with the last at 8:00 PM. Total Ldopa 1500 mg. But the last week or two I have started breaking the 2:00 PM and 4:00 PM in half which brings it down to 1300 mg. It also has pretty much eliminated dyskinesia, too.

I have mostly eliminated Requip and take a single 4mg tablet two or three times per week to stop leg cramps. I was taking 24 mg per day earlier this year.

I still take the propranderolol 40 mg, 3x daily. Since I had been taking it for several weeks before starting the perindopril, I thought it best, especially in light of my blood pressure.

Current BP is 149/102. Pulse is 62. It is early morning and I am running on coffee and the first med of the day. Some slight to medium DK says it may be time to break another pill.

I have not had a true "attack" in weeks (the totally incapacitating type lasting 2 to 4 hours which does not respond to PD meds. I credit the propranderolol and the perindopril, but I also am convinced that avoiding the insulin-stimulating carbs have been key. In fact, I would wager a considerable sum that a big, old jelly donut right now would paralyze me until lunchtime (get thee behind me Satan!)

To sum up, I continue to see wide improvement in all areas.

Laura-
Reread your post. Even though your BP is good, don't assume that it rules you out. I experienced a worsening of symptoms at first that may have been low BP. It would last two hours then everything was OK. By moving the dose to bedtime, however, I eliminated the problem completely.

Also, the suggested dose for BP is 8 mg daily. I am doing just fine on half that. And as MrsD pointed out, there are other ACE inhibitors to be tested as well.

Hi Reverett123,

Have been reading this thread with great interest. (This is my first post here.) Was dx'ed in May with YOPD after about eight years of mild symptoms. Haven't started meds yet, exercise keeps me going for now. Your comment about avoiding insulin producing carbs struck a cord. I was dx'ed with severe hypoglycemia (low blood sugar) 9 years ago at age 38. Then eliminated sugar, white flour, pasta, potatoes, chocolate, and alcohol. Kept to this diet for 5 years before starting new job. Within 6 months of lax eating habits began getting additional symptoms besides kinetic/postural tremor. And tremor plus handwriting worsened. Direct correlation? Over eating of sugar set off hypoglycemia and PD? Then strict diet kept symptoms very minimal, relaxed diet allowed PD to progress more quickly? I don't eat as much simple carbs as average person, but Will have to go back to strict diet and see what happens. What has your experience been that made you notice link? Thanks for this thread, hope you continue to see improvements on ACE med. Best wishes, Lin

Lin2-
Welcome aboard. Sorry you're here. :)
Sugar, etc might seem a little off topic for this thread, but then again...

Regarding what made me notice the link to insulin, it was a tornado. :D A couple of years ago, I was dealing with some major stressors. About the worst of a long string of bad ones. One night I found myself on the floor too weak to crawl. A couple of nights later, reports of a tornado approaching shot me full of adrenaline. I woke my wife and then collapsed completely. With an F5 twister bearing down, I couldn't lift an arm. Luckily the storm lifted, but I was left wondering about the vaunted power of adrenaline to give PWP super powers.

About the same time, I was having increasing trouble simply walking, especially first thing in the day. During all this a morning arrived when I could no longer stand. I was weak as the proverbial kitten.

My wife, in desperation, forced two potassium tablets on me. What followed was one of the stranger things that I have encountered. Long before those two tabs had cleared my mouth, my body somehow recognized them and began releasing what stores of potassium it had hoarded. How it knew, I have no idea. That it knew, I am certain. I was standing within thirty seconds.

This experience, understandably, led to some thinking. That led to the endocrine system, the most amazing part of the human body for my money. And I suspect, a major factor in PD.

I learned- Potassium is essential for nerve and muscle function. Too much or too little can stop your heart. So the amounts in your body are tightly controlled by a cascade of hormones such as aldosterone, angiotensin, and renin. But some of us produce too much. This can lead to the wholesale shift of potassium into the cells from the bloodstream.

This shift renders us unable to move and worsens our PD symptoms as well. These "attacks", as they are known, last from one to six hours and are most common in the afternoons. They involve a lot of bladder action and blood pressure swings.

Those of us who are born with or develop this vulnerability have certain things which act as triggers. The most common trigger is the insulin surge that comes from a high carb meal. The insulin causes the cells to suck up glucose. And potassium among those so prone.

So, what makes us prone? One thing is over-production of angiotensin. Perindopril seems to interupt that cascade.

But there is something more.

J Appl Physiol. 2004 Dec;97(6):2339-46. Epub 2004 Jul 16.
Levodopa with carbidopa diminishes glycogen concentration, glycogen synthase activity, and insulin-stimulated glucose transport in rat skeletal muscle.

Our "gold standard" medication can contribute to insulin resistance and increase the problems with the shifting potassium as we release greater amounts of insulin.

In other words, PD is a cousin to diabetes.

One other bit to add to this admittedly incomplete picture before I go- In 1973 the British Medical Journal publshed a paper on the then still new wonder drug levodopa-carbidopa. It was an investigation into what was known as the "On-Off Phenomenum". I will highlight the interesting bits-

From British Medical Journal; 17 February 1973 (Pg 373)

Levodopa has proved to -be safe despite many dose-
dependent adverse reactions at the start of treatment when
the dose is being adjusted to an optimal level. But with long-
term treatment two new problems have emerged. One,
which has been termed "oscillation in performance" or the
"on-off phenomenon," comprises rapid transient deteriora-
tion of the Parkinsonian motor deficit, which develops over
minutes and usually persist for 1-6 hours. These episodes
then clear spontaneously. Hypokinesia, tremor, and rigidity
may be exacerbated over the period of deterioration. Hypo-
tonia is common and has also lbeen reported. These
oscillations in performance are commonest in patients
who have been on levodopa for over a year. They usually
occur in the afternoon, and they may be repeated in cycles.
Their mechanism is not understood.....

clinical symptoms. Administration of levodopa over a year
has been found to result in a rise of growth hormone in the
plasma, an increase in serum cholesterol, a decrease in glu-
cose tolerance, and a delayed but exaggerated insulin re-
sponse.3 It appears that these changes take some time to
become established, as similar investigations after shorter
periods of levodopa therapy have failed to show the same
abnormalities.4

I could not have written a better description of what I was experiencing. And I do think it is a problem with levodopa and insulin.

Thanks for this. Your knowledge is amazing! Lin2

Blood Pressure
 

What if a person has all the same bouts and symptoms you describe, Reverett. Except, their blood pressure is low, as in sometimes 89/57 or 95/63 with a pulse rate anywhere from 65 to 90. Peripheral neuropathy is dominate, shortness of breath, all this when I'm "off".
Seems like BP has no involvement as a precurser. I think BP might be a result of what is going on in us. (I know, "duh")

I wake with all of those same symptoms. Then, meds work great, and after lunch, bad "off" time lasting hours.

I'm following with interest, too.

thanks so much!
Tonya

Tonya-
With the attacks that I am talking about my BP would swing that low. How high does yours go at the worst time? And what effect is there onyour "offs" if you skip lunch?
-Rick

Reverett,
At my worst time the BP is around 97/63 and pulse around 75 or more. If I skip lunch, off times seem to be worse. Puzzled about neuropathy. When meds work, I don't have it at all.

Thanks for the help.
Tonya

Possible Hypotension?

having a pretty bad "off" time now. just took BP
107/69 pulse 86

Sorry
 

Sorry, I should put these concerns and questions on a visitor's message.
I definitely don't want a big audience.

Please proceed with the subject at hand - Perindopril Test.

Thank you, Rick

Tonya

Update
 

Sorry that I have been letting this thread slip and I will try to bring it a little more up to date. I continue to be both leased and hopeful with the perindopril. No miracles but, instead, a sense of steady improvement. I keep tinkering with dosage and so on. This, in turn, is a little messy. But, heck, if you want tidy go out and buy a gerbil! :)

Earlier this evening, my wife mentioned that it has been a great relief to once again have my help around the house! Once she pointed it out I could see that, once I quit messing with times and dosages, there was an unmistakable improvement overall. I will do better on keeping this updated.

Of the three ACE inhibitors only trandopril (Mavik) is available in the US.
It is not commonly prescribed, though. The most common side effect of
drugs in this class is a cough. Rarely, they cause angioedema which can be fatal.

GerryW-
Wikipedia lists 14 individual ACEIs. They don't say which are not available in the US. I know that at least one is available (i.e. perindopril). So somewhere between the two. -Rick

I would like to remind here, that not ACE inhibitors cross the blood brain barrier well or at all. I have a post above that
has a link about that.

""ACE inhibitors that cross the blood-brain barrier reduce cognitive decline by 50% compared [with] the decline seen in people on other blood pressure medications," presenter and lead author Kaycee M. Sink, MD, MAS, an assistant professor of internal medicine in gerontology at Wake Forest University School of Medicine in Winston-Salem, North Carolina, told Medscape.

Centrally active ACEIs, such as captropril (Capoten), fosinopril (Monopril), lisinopril (Prinivil or Zestril), perindopril (Aceon), ramipril (Altace), and trandolapril (Mavik), cross the blood-brain barrier. Previous animal studies suggest that centrally active ACEIs protect against dementia not only by controlling hypertension, but also by decreasing oxidative stress and reducing inflammation in the brain.

"Treating blood pressure may be about more than just getting blood pressure to a certain target," Dr. Sink said. "Which drug we use may have implications beyond blood pressure control, like reducing risk of cognitive decline. High blood pressure is a risk factor for dementia, so it is important to know if the type of blood pressure medicine a person takes can cut that risk."

http://www.medscape.com/viewarticle/556014

Polyuria and Sodium
 

Rick,

As you know, I experience attacks very similar to yours. I am trying to understand how I have weakness, can barely walk, or speak, yet have a spike in blood pressure. I am normally at 109/80 and yesterday at height of a mild attack it was at 153/100 which scared the heck out of me. If my doctor does not address I honestly feel like I will not make it another five years. This feels so taxing on my system and I know must exacerbate, if not accelerate PD.

I am trying to narrow down whether it is my aldosterone levels, simply a side effect of levodopa, or a primary kidney dysfunction. I was hospitalized three years ago during my pregnancy for a pretty intense kidney infection. So I'd say I am having symptoms of renal tubular acidosis and/or diabetes insipidus as well as the renin-angiotensin deal.

Is polyuria a key element of the aldosterone overload? Does this result in too much sodium in our bloodstream and low potassium? Or do we lose both sodium and potassium through large volumes of urine. I can say I am urinating out way more liquid than I take in, feel parched/dehydrated most of the time, yet at the sam time crave salt. I get the blood pressure spike during an attack then normalize within minutes of urinating.

Sorry to be so graphic...TMI for most. Normally, I'd PM you but I suspect there are many more off us going through this, so doing my part to hopefully help others.

Thanks!

Laura