Role of angiotensin II in chronic intermittent hypoxia-induced hypertension and cognitive decline.
Alexandria B MarcianteBrent ShellGeorge E FarmerThomas J CunninghamPublished in: American journal of physiology. Regulatory, integrative and comparative physiology (2021)
Sleep apnea is characterized by momentary interruptions in normal respiration and leads to periods of decreased oxygen, or intermittent hypoxia. Chronic intermittent hypoxia is a model of the hypoxemia associated with sleep apnea and results in a sustained hypertension that is maintained during normoxia. Adaptations of the carotid body and activation of the renin-angiotensin system may contribute to the development of hypertension associated with chronic intermittent hypoxia. The subsequent activation of the brain renin-angiotensin system may produce changes in sympathetic regulatory neural networks that support the maintenance of the hypertension associated with intermittent hypoxia. Hypertension and sleep apnea not only increase risk for cardiovascular disease but are also risk factors for cognitive decline and Alzheimer's disease. Activation of the angiotensin system could be a common mechanism that links these disorders.
Keyphrases
- sleep apnea
- cognitive decline
- blood pressure
- angiotensin ii
- mild cognitive impairment
- high intensity
- positive airway pressure
- obstructive sleep apnea
- cardiovascular disease
- angiotensin converting enzyme
- endothelial cells
- neural network
- white matter
- vascular smooth muscle cells
- transcription factor
- multiple sclerosis
- coronary artery disease
- cardiovascular risk factors
- brain injury
- arterial hypertension