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Journal Article: Adventitial Fibroblasts In Vascular Structure And Function: The Role Of Oxidative Stress And Beyond


Crow

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http://tinyurl.com/3ajxzr7

Can. J. Physiol. Pharmacol. 88(3): 177?186 (2010) | doi:10.1139/Y10-015

From what I understand, a fibroblast = a cell that helps make collagen (? or is it a component of it?) so perhaps the adventitia is the culprit in secondary POTS from Ehlers-Danlos syndrome. (Fig 1 "The anatomy and cellular composition of the blood vessel.")

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I read the whole thing, but most of it was Greek to me. And I'm not Greek. But, from what I get from it. It seems that this produces more collagen, which would be more indicative of Scleroderma. In this illness, there is too much collagen and the tissues get really stiff and hard. Sometimes the skin will split and they have to massage it with creams to keep it supple. With Ehlers Danlos, there is a collagen problem but it doesn't cause tightness, but laxness. It's sort of the opposite. This particular study may still be relative, but my feelings is it would apply more to scleroderma.

Ehlers Danlos has been in fact proven to cause POTS issues in people. I'm one of those.

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This is a good article.

I suppose from this perspective that EDSers blood vessels aren't "stretchy" but "loose" instead. "Loose" when they should be stiffer.

If excessive collagen deposition leads to vascular stiffness and hypertensive states, then perhaps deposition of diminished or otherwise abnormal collagen leads to looseness, lowered blood pressure and the kind of autonomic dysfunction that EDS patients exhibit.

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