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Published on: November 2, 2015
Endothelin 1-dependent neurovascular dysfunction in chronic intermittent hypoxia.
Carmen Capone1, Giuseppe Faraco, Christal Coleman
1Division of Neurobiology, Department of Neurology and Neuroscience, College of Veterinary Medicine, Cornell University, Ithaca, NY, USA.
Hypertension (Dallas, Tex. : 1979)
|June 13, 2012
Summary
Chronic intermittent hypoxia (CIH) from sleep apnea impairs brain blood flow regulation. This dysfunction, driven by endothelin 1 and oxidative stress, increases stroke risk by reducing cerebrovascular reserves.
Area of Science:
- Neuroscience
- Cardiovascular Science
- Sleep Medicine
Background:
- Obstructive sleep apnea (OSA) is linked to stroke and dementia.
- Mechanisms connecting OSA-induced chronic intermittent hypoxia (CIH) to cerebrovascular risk are unclear.
Purpose of the Study:
- To investigate if CIH alters cerebral blood flow regulation, reducing cerebrovascular reserves.
- To identify molecular pathways involved in CIH-induced cerebrovascular dysfunction.
Main Methods:
- Mice were exposed to CIH or sham conditions for 35 days.
- Cerebral blood flow was measured using laser Doppler flowmetry.
- Vascular function, oxidative stress, endothelin 1, and NADPH oxidase activity were assessed.
Main Results:
- CIH increased blood pressure and attenuated blood flow responses to neural and vasodilator stimuli.
- Cerebrovascular dysfunction was linked to oxidative stress via NADPH oxidase (NOX2 subunit) and increased endothelin 1.
- Inhibition of free radicals, NADPH oxidase, or endothelin A receptors reversed CIH effects.
Conclusions:
- CIH impairs cerebral blood flow regulation through endothelin 1 and NADPH oxidase-derived radicals.
- This dysfunction reduces cerebrovascular reserves, potentially increasing stroke risk in sleep apnea patients.
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