Aldosterone Actually Decreases Sodium

[Estradiol]

The title is little tricky.

Aldosterone known to cause sodium retention and potassium depletion. This maybe true for blood but not cellular.

Na-K-ATPase is an enzyme that responsible for promoting potassium, depleting sodium.

This study shows that aldosterone actually increased Na-K-ATPase enzyme and decreased intracellular sodium. Spironolactone blocked this effect and promoted intracellular sodium.

Digoxin, another heart failure drug, known to inhibit Na-K-ATPase and promote sodium retention.


Effect of Spironolactone on Cytosolic Free Sodium Concentration in Platelets From Hypertensive Patients With Primary Aldosteronism - PubMed

[Na+]i was significantly decreased in platelets from patients with primary aldosteronism compared to control subjects.

From the present results it may be concluded that intracellular sodium is decreased by aldosterone-induced activation of Na-K-ATPase. That activation may be partly blocked by spironolactone.

 

[mrchibbs]

The title is little tricky.

Aldosterone known to cause sodium retention and potassium depletion. This maybe true for blood but not cellular.

Na-K-ATPase is an enzyme that responsible for promoting potassium, depleting sodium.

This study shows that aldosterone actually increased Na-K-ATPase enzyme and decreased intracellular sodium. Spironolactone blocked this effect and promoted intracellular sodium.

Digoxin, another heart failure drug, known to inhibit Na-K-ATPase and promote sodium retention.


Effect of Spironolactone on Cytosolic Free Sodium Concentration in Platelets From Hypertensive Patients With Primary Aldosteronism - PubMed

[Na+]i was significantly decreased in platelets from patients with primary aldosteronism compared to control subjects.

From the present results it may be concluded that intracellular sodium is decreased by aldosterone-induced activation of Na-K-ATPase. That activation may be partly blocked by spironolactone.

I could not be understanding, but I thought that was the understood relationship. Dietary salt lowers aldosterone. Spironolactone, taking on the characteristic of the original molecule, is aldosterone antagonist. Ray said that progesterone is the "opposite" of aldosterone in the ORN interview in May. He referred to aldosterone as the "brittlizing" hormone. So it make sense that spironolactone would increase intracellular sodium. (not sure what he meant lol) Spiro is a very interesting drug.

 

[Estradiol]

I could not be understanding, but I thought that was the understood relationship. Dietary salt lowers aldosterone. Spironolactone, taking on the characteristic of the original molecule, is aldosterone antagonist. Ray said that progesterone is the "opposite" of aldosterone in the ORN interview in May. He referred to aldosterone as the "brittlizing" hormone. So it make sense that spironolactone would increase intracellular sodium. (not sure what he meant lol) Spiro is a very interesting drug.

Correct.

Salt reduces aldosterone and potassium increases it.

Spironolactone increases potassium so plasma aldosterone will raise. But it's effects will be blocked.

Receptor antagonism usually ends up with increases in blood levels. So it's not a good way.

You need the inhibit aldosterone synthase from root. So it won't activate the receptor nor increase blood values.

 

[Tristan Loscha]

Effect of aldosterone and mineralocorticoid receptor blockade on vascular inflammation
Hylton V Joffe, Gail K Adler
Heart failure reviews 10 (1), 31-37, 2005
Aldosterone, the final product of the renin-angiotensin-aldosterone system, is classically viewed as a regulator of renal sodium and potassium handling, blood volume, and blood pressure. Recent studies suggest that aldosterone can cause microvascular damage, vascular inflammation, oxidative stress and endothelial dysfunction. In animal models, aldosterone-mediated vascular injury in the brain, heart, and kidneys leads to stroke, myocardial injury, and proteinuria. These effects may be modified by dietary salt intake; aldosterone-mediated vascular damage is increased in susceptible animals fed a high-salt diet compared to a low-salt diet despite lower plasma aldosterone levels on the high-salt diet. In humans, there is a growing literature supporting the adverse effects of aldosterone in heart failure, hypertension, left ventricular hypertrophy, and renal disease. Aldosterone receptor antagonists are beneficial even in patients on angiotensin converting enzyme inhibitors and attenuate aldosterone-mediated vascular injury by mechanisms that appear to be independent of changes in systolic blood pressure. This review focuses on the adverse effects of aldosterone on the vascular system and describes our current understanding of the underlying mechanisms for this injury.

 

[GorillaHead]

https://www.ahajournals.org/doi/pdf/10.1161/01.HYP.14.2.164

I just shared this earlier. Finding ways to reduce aldosterone synthase is very tough.

 

[Hgreen56]

so what i understand is: the Ray peat diet is a high potassium diet = high aldosterone = microvascular damage, vascular inflammation, oxidative stress, endothelial dysfunction.
And so this is way people notice strength loss on high potassium diet?

Ive noticed a loss in strength when my potassium is high in comparison to sodium. Especially when eating a lot of bananas.

i miss something here?
this sound not really healthy.

i also wondering what @tca300 thinks about this, because you drinks tons of milk and you hit probably 8+ grams potassium a day.
You consume the same amount or more sodium?

 

[jb116]

Aldosterone as an acute regulator - and that's just in case potassium gets out of control, not easy with diet - is fine. It is akin to cortisol regulating blood sugar in an emergency. It's chronic elevation of these stress hormones that pose problems. There is a necessary understanding here of correlation and direct causation. In cases of chronic or prolonged hyperkalemia, the correlation of the dangers of aldosterone have to do more with the fact there is renal failure for example or tumor lysis as another, in which potassium is of course elevated. In other words, there is true hyperkalemia indicating a very poor metabolic state or ill state in which aldosterone will be prolonged and chronic. Not a good situation.