The DOI matches its Crossref record; 218 of the 219 references it cites were found in a registry or an index.
Role of neurons and glia in the CNS actions of the renin-angiotensin system in cardiovascular control
Open accessAbstract
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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“and the central renin-angiotensin system has an important role in mediating neuroinflammation174.”
From The gut microbiota and the brain–gut–kidney axis in hypertension and chronic kidney disease (2018) · cites this paper as [174]
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Metadata
- 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
- 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
- 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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