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Neurovascular Coupling in Hypertension Is Impaired by IL-17A through Oxidative Stress
Jessica Youwakim1,2,3,4, Diane Vallerand1, Helene Girouard1,2,3,4
1Département de Pharmacologie et Physiologie, Université de Montréal, Montreal, QC H3T 1J4, Canada.
International Journal of Molecular Sciences
|February 25, 2023
Summary
Interleukin-17A (IL-17A) links hypertension to neurodegenerative diseases by impairing cerebral blood flow regulation. Blocking IL-17A may restore cerebrovascular function in hypertension.
Area of Science:
- Neuroscience
- Cardiovascular Science
- Immunology
Background:
- Hypertension is a chronic inflammatory condition linked to neurovascular and neurodegenerative diseases like stroke and Alzheimer's.
- Elevated interleukin-17A (IL-17A) levels are associated with these neurological conditions.
- Cerebral blood flow regulation, particularly neurovascular coupling (NVC), may be a key link between hypertension and neurodegeneration.
Purpose of the Study:
- To investigate the role of IL-17A in hypertension-induced impairment of NVC.
- To determine if IL-17A mediates cerebrovascular dysfunction caused by angiotensin II (Ang II).
Main Methods:
- Examined the effects of IL-17A neutralization and receptor inhibition on Ang II-induced NVC impairment in a hypertension model.
- Assessed the impact of chronic IL-17A administration on NVC and cerebral superoxide production.
- Utilized Tempol treatment and NADPH oxidase 2 gene deletion to investigate the role of superoxide anions.
Main Results:
- IL-17A neutralization or receptor inhibition prevented Ang II-induced NVC impairment and superoxide production.
- Chronic IL-17A administration impaired NVC and increased superoxide production.
- Tempol and NADPH oxidase 2 gene deletion reversed the effects of IL-17A on NVC and superoxide production.
Conclusions:
- IL-17A is a significant mediator of Ang II-induced cerebrovascular dysregulation in hypertension.
- IL-17A exerts its effects through increased superoxide anion production.
- Targeting the IL-17A pathway offers a potential therapeutic strategy for restoring cerebrovascular regulation in hypertensive individuals.
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