AI Article Synopsis
- Rats with a neurodegenerative disorder showed impaired dilation of brain blood vessels due to reduced endothelial NO production from a toxic beta-amyloid fragment.
- This toxic fragment also caused the formation of NO deposits in vessel walls, indicating an imbalance in NO production in brain tissue.
- Adapting to low oxygen levels (hypoxia) helped prevent endothelial dysfunction and improved NO storage, suggesting a protective mechanism against neurodegenerative damage.
Article Abstract
The rats with neurodegenerative brain disorder induced by administration of a toxic fragment of beta-amyloid demonstrate weakened endothelium-dependent dilation of cerebral vessels, which attested to impaired production of endothelial NO. At the same time, toxic beta-amyloid fragment induced the formation of NO depots in the walls of cerebral vessels, which indirectly attests to NO overproduction in the brain tissue. Preadaptation to hypoxia prevented endothelial dysfunction and improved the efficiency of NO storage. Our results suggest that adaptation to hypoxia protects the brain from various changes in NO production during neurodegenerative damage.
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| http://dx.doi.org/10.1007/s10517-006-0318-6 | DOI Listing |
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