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Hypertension and Brain Inflammation: Role of RAS-Induced Glial Activation

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Hypertension and the Brain as an End-Organ Target

Abstract

Increasing evidence indicates a strong association between inflammatory processes within brain cardiovascular control centers and hypertension that is neurogenic in origin.

On the one hand, evidence exists that neuroinflammatory mechanisms play a pivotal role in the development and maintenance of neurogenic hypertension, while on the other hand chronic hypertension causes systemic inflammation that can lead to enhancement of neuroinflammatory processes in cardiovascular control centers of the brain. In this review we discuss the evidence for both of these points of view. Further, we discuss the data that point to an active role of the intrinsic renin-angiotensin system (RAS) within cardiovascular regulatory centers of the brain in the neuroinflammatory processes that contribute to neurogenic hypertension, with particular emphasis on the involvement of microglia and astrocytes in these mechanisms. We have developed and present here a hypothetical model of such interactions.

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Correspondence to Colin Sumners .

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Rodríguez, V., de Kloet, A.D., Sumners, C. (2016). Hypertension and Brain Inflammation: Role of RAS-Induced Glial Activation. In: Girouard, H. (eds) Hypertension and the Brain as an End-Organ Target. Springer, Cham. https://doi.org/10.1007/978-3-319-25616-0_9

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