Please watch my youtube video.
http://www.youtube.com/watch?v=QOCtf4zsdeI
http://www.youtube.com/watch?v=QOCtf4zsdeI
ANP, the link between low blood volume and Сhronic Fatigue Syndrome?
- Thread starter Emootje
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Wow! Thank you, Emootje.
Merry
Merry
very interesting.....would it be possible for you to put the first couple of minutes (the explanation part) on here in writing?
It is possible:
Atrial natriuretic peptide is a natural diuretic that is produced in the atrium of the heart.
For example:
When you eat soup, your blood volume expanse and your heart is getting larger. This causes the atrial walls to stretch.
It then releases atrial natriuretic peptide, whit’s travels to the bloodstream to the kidney, wit’s then causes the kidney to produce more urine, that will normalize your blood volume and your atrial natriuretic peptide levels again.
In some disease the body is fooled to think there is too much fluid in the body.
These disease are almost all characterized by an increase in endothelin-1, a vasoconstrictor and a potent atrial natriuretic peptide stimulator.
This activation of the endothelin-1/atrial natriuretic peptide pathway results in chronic low blood volume.
The endothelin-1/atrial natriuretic peptide pathway is stimulated by:
Oxidative stress such as isoprostanes and oxidized low-density lipoproteins
Inflammation factors such as interleukin-1, interleukin-3, tumor necrosis factor alpha, interferon gamma, transforming growth factor beta and endotoxin.
Hypoxia
Some examples of diseases with increased endotelin-1/atrial natriuretic peptide pathway activation and hypovolemia are: biliary obstruction, sleep apnea, chronic obstructive pulmonary disease with hypoxia and septic shock.
Chronic fatigue syndrome is characterized by low blood volume, cytokines abnormalities, oxidative stress and a low peak oxygen consumption. This low blood volume could be explained by high atrial natriuretic peptide levels stimulated by inflammation, hypoxia or oxidative stress.
Emootje
Atrial natriuretic peptide is a natural diuretic that is produced in the atrium of the heart.
For example:
When you eat soup, your blood volume expanse and your heart is getting larger. This causes the atrial walls to stretch.
It then releases atrial natriuretic peptide, whit’s travels to the bloodstream to the kidney, wit’s then causes the kidney to produce more urine, that will normalize your blood volume and your atrial natriuretic peptide levels again.
In some disease the body is fooled to think there is too much fluid in the body.
These disease are almost all characterized by an increase in endothelin-1, a vasoconstrictor and a potent atrial natriuretic peptide stimulator.
This activation of the endothelin-1/atrial natriuretic peptide pathway results in chronic low blood volume.
The endothelin-1/atrial natriuretic peptide pathway is stimulated by:
Oxidative stress such as isoprostanes and oxidized low-density lipoproteins
Inflammation factors such as interleukin-1, interleukin-3, tumor necrosis factor alpha, interferon gamma, transforming growth factor beta and endotoxin.
Hypoxia
Some examples of diseases with increased endotelin-1/atrial natriuretic peptide pathway activation and hypovolemia are: biliary obstruction, sleep apnea, chronic obstructive pulmonary disease with hypoxia and septic shock.
Chronic fatigue syndrome is characterized by low blood volume, cytokines abnormalities, oxidative stress and a low peak oxygen consumption. This low blood volume could be explained by high atrial natriuretic peptide levels stimulated by inflammation, hypoxia or oxidative stress.
Emootje
Thank you for the information!
Thanks, very interesting. Is there a test for endothelin-1 levels, do you know?
There is an ELISA endothelin-1 test.
for example: http://www.rndsystems.com/pdf/bbe5.pdf
for example: http://www.rndsystems.com/pdf/bbe5.pdf
Thank you!! : )
The Kennedy group found no elevation of ET-1 in CFS:
http://rheumatology.oxfordjournals.org/content/43/2/252.full.pdf+html
Still thinking that ANP plays a major role in ME/CFS's volume depletion. Prostaglandins (PGF2 alpha, PGE2) and oxidative stress (MAPK p38, PKC) can increase ANP without increasing ET-1.
http://cardiovascres.oxfordjournals.org/content/cardiovascres/68/1/8.full.pdf
http://rheumatology.oxfordjournals.org/content/43/2/252.full.pdf+html
Still thinking that ANP plays a major role in ME/CFS's volume depletion. Prostaglandins (PGF2 alpha, PGE2) and oxidative stress (MAPK p38, PKC) can increase ANP without increasing ET-1.
http://cardiovascres.oxfordjournals.org/content/cardiovascres/68/1/8.full.pdf
Interesting about what increases ANP. I watched your "Factors that increase ANP" video, and I'm a bit confused about how specifically these factors affect ANP. For instance, vasopressin. Is it elevated ADH that affects ANP increase? Or is it decreased ADH that affects it?
I've been tested for everything on your list in the video except endothelin-1 and isoprostanes. Everything is in the normal range except for vasopressin/ADH, which is always almost non-existent, and transforming growth factor beta, specifically TGF-B1, which is always at least five times higher than the upper normal range limit, like most of Shoemaker's patients.
Since ANP inhibits renin secretion, this would easily explain why my renin values are always below normal when measured. My aldosterone and angiotensin II are in the normal range, but not renin. And having elevated ANP would readily explain this.
I've been tested for everything on your list in the video except endothelin-1 and isoprostanes. Everything is in the normal range except for vasopressin/ADH, which is always almost non-existent, and transforming growth factor beta, specifically TGF-B1, which is always at least five times higher than the upper normal range limit, like most of Shoemaker's patients.
Since ANP inhibits renin secretion, this would easily explain why my renin values are always below normal when measured. My aldosterone and angiotensin II are in the normal range, but not renin. And having elevated ANP would readily explain this.
I note that
Maybe this means that they were relatively well-rested. Perhaps levels would be different after exertion?
This page says that ET-1
The aldosterone would be anti-natriuretic and anti-diuretic. So ET-1 regulates these according to conditions?
Maybe this means that they were relatively well-rested. Perhaps levels would be different after exertion?
This page says that ET-1
The aldosterone would be anti-natriuretic and anti-diuretic. So ET-1 regulates these according to conditions?
@MeSci: I guess that ANP protects the heart (at the expense of blood volume) from to much pressure from potent vasoconstrictors like ET-1.
@out2lunch: Vasopressin increases ET-1 (table 1) so I guess that elevated ADH will stimulate ANP secretion.
On the other hand, in this review they mentioned that ANP inhibit vasopressin release.
Interesting about your low renin values, POTS patients have also low renin values and in this study they noted that ANP or dopamine could be the cause of this low renin. Normally if renin is low, the downstream hormones (angiotensin II and aldosterone) are also low, so that is a little bit weird that your aldosterone and angiotensin II are in the normal range. Lastly, transforming growth factor beta can activate MAPK p38 and vise versa. Inhibiting MAPK p38 could theoretical be helpful to lower ANP.
@out2lunch: Vasopressin increases ET-1 (table 1) so I guess that elevated ADH will stimulate ANP secretion.
On the other hand, in this review they mentioned that ANP inhibit vasopressin release.
Interesting about your low renin values, POTS patients have also low renin values and in this study they noted that ANP or dopamine could be the cause of this low renin. Normally if renin is low, the downstream hormones (angiotensin II and aldosterone) are also low, so that is a little bit weird that your aldosterone and angiotensin II are in the normal range. Lastly, transforming growth factor beta can activate MAPK p38 and vise versa. Inhibiting MAPK p38 could theoretical be helpful to lower ANP.