title: Role of neurons and glia in the CNS actions of the renin-angiotensin system in cardiovascular control.
abstract: Despite tremendous research efforts, hypertension remains an epidemic health concern, leading often to the development of cardiovascular disease. It is well established that in many instances, the brain plays an important role in the onset and progression of hypertension via activation of the sympathetic nervous system. Further, the activity of the renin-angiotensin system (RAS) and of glial cell-mediated proinflammatory processes have independently been linked to this neural control and are, as a consequence, both attractive targets for the development of antihypertensive therapeutics. Although it is clear that the predominant effector peptide of the RAS, ANG II, activates its type-1 receptor on neurons to mediate some of its hypertensive actions, additional nuances of this brain RAS control of blood pressure are constantly being uncovered. One of these complexities is that the RAS is now thought to impact cardiovascular control, in part, via facilitating a glial cell-dependent proinflammatory milieu within cardiovascular control centers. Another complexity is that the newly characterized antihypertensive limbs of the RAS are now recognized to, in many cases, antagonize the prohypertensive ANG II type 1 receptor (AT1R)-mediated effects. That being said, the mechanism by which the RAS, glia, and neurons interact to regulate blood pressure is an active area of ongoing research. Here, we review the current understanding of these interactions and present a hypothetical model of how these exchanges may ultimately regulate cardiovascular function.
authors.affiliation: Department of Physiology and Functional Genomics, and McKnight Brain Institute, University of Florida College of Medicine, Gainesville, Florida; and.
authors.forename: Annette D
authors.initials: AD
authors.lastname: de Kloet
authors.affiliation: Department of Physiology and Functional Genomics, and McKnight Brain Institute, University of Florida College of Medicine, Gainesville, Florida; and.
authors.forename: Meng
authors.initials: M
authors.lastname: Liu
authors.affiliation: Department of Physiology and Functional Genomics, and McKnight Brain Institute, University of Florida College of Medicine, Gainesville, Florida; and.
authors.forename: Vermalí
authors.initials: V
authors.lastname: Rodríguez
authors.affiliation: Department of Pharmacodynamics, University of Florida College of Pharmacy, Gainesville, Florida.
authors.forename: Eric G
authors.initials: EG
authors.lastname: Krause
authors.affiliation: Department of Physiology and Functional Genomics, and McKnight Brain Institute, University of Florida College of Medicine, Gainesville, Florida; and csumners@ufl.edu.
authors.forename: Colin
authors.initials: C
authors.lastname: Sumners
mesh_terms: D000804:Angiotensin II / Q000378:metabolism; D000818:Animals; D001794:Blood Pressure; D002319:Cardiovascular System / Q000294:innervation / Q000378:metabolism*; D002450:Cell Communication; D002490:Central Nervous System / Q000378:metabolism* / Q000503:physiopathology; D006801:Humans; D006973:Hypertension / Q000378:metabolism* / Q000503:physiopathology; D009457:Neuroglia / Q000378:metabolism*; D009474:Neurons / Q000378:metabolism*; D044140:Receptor, Angiotensin, Type 1 / Q000378:metabolism; D012084:Renin-Angiotensin System
chemical_list: D044140:Receptor, Angiotensin, Type 1; D000804:Angiotensin II
keywords: angiotensin II; astrocyte; microglia; neurogenic hypertension; renin