IL-17A Contributes to the Angiotensin II-induced Neurovascular Coupling impairment through Oxidative Stress

Hypertension, a multifactorial chronic inflammatory condition, is a risk factor for neurodegenerative diseases including stroke and Alzheimer’s disease. These diseases have been associated with higher concentration of blood interleukin (IL)-17A. However, the role that IL-17A plays in the relationship between hypertension and brain remains misunderstood. Cerebral blood flow regulation may be the crossroads of these conditions. Hypertension alters cerebral blood flow regulation including neurovascular coupling (NVC). In the present study, the effects of IL-17A on NVC in the context of hypertension induced by angiotensin (Ang) II will be examined. Our results show that the neutralization of IL-17A or the specific inhibition of its receptor prevent the Ang II- induced NVC impairment. These treatments reduce the Ang II-induced cerebral oxidative stress. Tempol and NOX-2 depletion prevent NVC impairment induced by IL-17A. These findings suggest that IL-17A, through superoxide anion production, is an important mediator of cerebrovascular dysregulation induced by Ang II.