Neuroinflammation in hypertension: the renin-angiotensin system versus pro-resolution pathways

Abstract

Overstimulation of the pro-inflammatory pathways within brain areas responsible for sympathetic outflow is well evidenced as a primary contributing factor to the establishment and maintenance of neurogenic hypertension. However, the precise mechanisms and stimuli responsible for promoting a pro-inflammatory state are not fully elucidated. Recent work has unveiled novel compounds derived from omega-3 polyunsaturated fatty acids (ω-3 PUFAs), termed specialized pro-resolving mediators (SPMs), which actively regulate the resolution of inflammation. Failure or dysregulation of the resolution process has been linked to a variety of chronic inflammatory and neurodegenerative diseases. Given the pathologic role of neuroinflammation in the hypertensive state, SPMs and their associated pathways may provide a link between hypertension and the long-standing association of dietary ω-3 PUFAs with cardioprotection. Herein, we review recent progress in understanding the RAS-driven pathophysiology of neurogenic hypertension, particularly in regards to the chronic low-grade neuroinflammatory response. In addition, we examine the potential for an impaired resolution of inflammation process in the context of hypertension.

Keywords: AVE0991 (PubChem CID: 78357809); Angiotensin (1–7) (PubChem CID: 71434130); Angiotensin 1-7; Angiotensin II; Angiotensin II (PubChem CID: 172198); BML-111 (PubChem CID: 10899465); Captopril (PubChem CID: 44093); Hydralazine (PubChem CID: 3637); LXA4-ME (PubChem CID: 5280914); Losartan (PubChem CID: 3961); Minocycline (PubChem CID: 54675783); RAS; central nervous system; hypertension; mitoTEMPO (PubChem CID: 135653355); resolution of inflammation.