Cited by 64Renin-Angiotensin System StudiesHeart Rate Variability and Autonomic ControlEicosanoids and Hypertension Pharmacology

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Role of neurons and glia in the CNS actions of the renin-angiotensin system in cardiovascular control

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de Kloet, Annette D., Liu, Meng, Rodríguez, Vermalí, Krause, Eric G., Sumners, Colin·2015·American Journal of Physiology-Regulatory, Integrative and Comparative Physiology

DOI 10.1152/ajpregu.00078.2015PMC PMC4591381

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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 (AT 1 R)-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.

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Authors: de Kloet, A. D., Liu, M., Rodríguez, V., Krause, E. G., & Sumners, C.
Affiliations: Department of Physiology and Functional Genomics, and McKnight Brain Institute, University of Florida College of Medicine, Gainesville, Florida; and
University of Florida Health (US)
Corresponding author: Sumners, Colin
ORCID: Liu, Meng
Krause, Eric G.
Sumners, Colin
Venue: American Journal of Physiology-Regulatory, Integrative and Comparative Physiology
Publisher: American Physiological Society
Published: 2015-09
Volume: 309
Issue: 5
Pages: R444-R458
ISSN: 0363-6119 (ISSN-L)
1522-1490
DOI: 10.1152/ajpregu.00078.2015
PMC: PMC4591381
OpenAlex: W2198204313
Cited by: 64
References: 219
Citations by year: 2026: 1 · 2024: 5 · 2023: 7 · 2022: 8 · 2021: 7 · 2020: 6 · 2019: 6 · 2018: 9 · 2017: 5 · 2016: 9 · 2015: 1
FWCI: 1.38
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Locations: American Journal of Physiology-Regulatory, Integrative and Comparative Physiology (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Funders: HHS | NIH | National Heart, Lung, and Blood Institute (NHBLI) (HL-033610, HL-096830, HL-093186, F32-HL-116074, HL-076803, K99-HL-125805)
Topics: Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Renin-Angiotensin System Studies
Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Heart Rate Variability and Autonomic Control
Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Eicosanoids and Hypertension Pharmacology
Keywords: renin-angiotensin system, angiotensin II, angiotensin II type 1 receptor, glial cells, microglia, neurons, blood pressure regulation, hypertension, cardiovascular regulation, neuroinflammation, antihypertensive peptides, central nervous system
MeSH terms: Angiotensin II, Animals, Blood Pressure, Cardiovascular System, Cell Communication, Central Nervous System, Humans, Hypertension, Neuroglia, Neurons, Renin-Angiotensin System, Receptor, Angiotensin, Type 1

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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

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Role of neurons and glia in the CNS actions of the renin-angiotensin system in cardiovascular control

Abstract

Overview

Integrity signals

Verification

Claims the paper makes

Claims other papers make about this one

Citations

Cites

Cited by

Related

Metadata

Record

About these checks