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http://www.sciencedaily.com/releases/2011/12/111214144751.htm

While this article is not about POTS, the heart brain connection is clearly there. What if the salt that is suggested is acting in a way other than increasing blood volume?

"Brain sends wrong message to heart

"We showed that the heart problems were actually secondary to nervous system deficits and that cardiac activity can be remolded by abnormalities in brain activity," said Neul. "Basically, the brain is sending the wrong message to the heart leading to the malfunction."

Taking a closer look at the heart cells affected by the nervous system deficits, researchers found an unusual persistent sodium current.

Sodium currents occur naturally in cell function. When there is cell activity, sodium travels in and out of the cell through a channel that acts like a window opening and closing. Unusual persistent sodium current means the "window" doesn't close properly, causing a slow trickle of sodium to flow through the channel for a longer period of time.

Seizure drug improves sodium problem

There are seizure medications that block this process, which also occurs in other neurological disorders. When Neul and his colleagues used an anti-seizure drug to treat these malfunctioning heart muscle cells in the lab, the sodium current problem improved. They then gave the common anti-seizure drug to the abnormal mice which corrected the heart rhythm problem and blocked sudden cardiac death."

There are parts that definitely missing in research and I think that a malfunction much like the one described will be the underlying issue for POTS.

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Interesting info. It would seem that in this situation, salt loading would make the problem worse? Or maybe not, since blood levels of sodium seem to be fairly tightly controlled in general?

Thanks for posting.

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Thanks for your post. Interesting. I have tried several cardiac and anticonvulsant drugs and the best ones for me by a long shot have been sodium channel blockers. Whilst neither is prescribed for POTS, I am sure they are helping my POTS symptoms.

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Cath_UK, I looked up sodium channel blockers based on your post and found this info:

Sodium channel blockers are agents that impair conduction of sodium ions (Na+) through sodium channels.

Sodium channel blockers are used in the treatment of cardiac arrhythmia. They are classified as "Type I" in the Vaughan Williams classification.

Class I antiarrhythmic agents interfere with the (Na+) channel. Class I agents are grouped by their effect on the Na+ channel, and by their effect on cardiac action potentials. Class I agents are called Membrane Stabilizing Agents. 'Stabilizing' refers to the decrease of excitogenicity of the plasma membrane effected by these agents. A few class II agents, propranolol for example, also have a membrane stabilizing effect.

Membrane stabilizing effects involve the inhibition or total abolishing of action potential from being propagated across the membrane. This phenomenon is common in nerve tissues as they are the carrier of impulses from the periphery to the central nervous system. Membrane stabilization is the method through which local anesthetics work. They block the propagation of action potentials across the nerve cell thereby producing a nerve block.

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I've questioned the use of salt for almost 2 years now. It seems like since it will lower aldesterone levels so low and ours are already low - it would cause us to be more dehydrated in the long run - because aldesterone is what balances out our fluid levels. (There is allot more to it than this simple statement. But, you get my drift of what I'm saying.)

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I've questioned the use of salt for almost 2 years now. It seems like since it will lower aldesterone levels so low and ours are already low - it would cause us to be more dehydrated in the long run - because aldesterone is what balances out our fluid levels. (There is allot more to it than this simple statement. But, you get my drift of what I'm saying.)

I agree. I don't even do the extra salt thing because it makes me soooooo thirsty it seems completely counter productive to me. I feel like salt loading is only useful if you have orthostatic hypotension, not hypertension. IMHO :)

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What if the "dumping" polyuria is the brain's mistaken attempt to increase serum sodium levels to compensate for a sodium-channel glitch? Could this be why propranolol works at such a low dose for many of us?

I do not salt load like most of you, I only take in enough to counteract the effects of the dDAVP. I am actually on a low-sodium diet based on the current medical viewpoint.

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thanks for posting this. I have a seizure disorder, oh and pots so maybe I should try this.

I started salt loading in 2007-8, after noticing at two docs appts weeks apart, that my bp was too low, 70\50.

It's never helped my oh or pots, but it keeps my bp up. I can only handle 2500 daily tho. I feel

too salty otherwise.

Just out of curiosity, wouldn't potassium be important here too ? My potassium is usually on the

low side of normal.

Oh and according to my new lab, blood draw, my aldosterone is good. It was 11 on a scale of 3 - 16.

I don.t have polyurea anymore as long as I treat with azo at the first sign. I have kidney stones tho,

so I suspect my polyuria is related to an oxalate problem.

tc .. D

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Yeah, I was actually told not to salt load. My sodium levels are always on the high side.

For the question about potassium - there is a study using Lorsartan which is a form of potassium and it is helping some. I'm in the experiment stage with it right now. Too soon to report my results.

Issie

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