Faculty Articles
Neuroinflammation and Sympathetic Overactivity: Mechanisms and Implications in Hypertension
Publication Title
Autonomic Neuroscience: Basic & Clinical
ISSN
1566-0702
Publication Date
3-1-2018
Keywords
brainstem, hypertension, neuroinflammation, renin angiotensin system, spontaneously hypertensive rats, sympathetic activity
Abstract
Essential hypertension is a multifactorial disorder with a strong genetic predisposition. Although anti-hypertensive medications have drastically reduced cardiovascular diseases mortality and morbidity rates, a significant percentage of hypertensive individuals currently on anti-hypertensive therapy, remain hypertensive. In spite of the emergence of transgenic animals and sophisticated tools to study the pathophysiology of hypertension, unraveling the causal mechanisms remains a challenge. Research on borderline hypertensive humans and/or prehypertensive rat models revealed an elevation in centrally-mediated sympathetic activity and a heightened neuroinflammatory state. Hyperactive brain renin angiotensin system (RAS), oxidative stress and neuroinflammation in brainstem cardiovascular centers and other brain regions are implicated as key factors in augmenting sympathetic activity in hypertension and other cardiovascular abnormalities. Angiotensin (Ang) II, the main RAS effector peptide, has been shown to trigger significant upsurges in pro-inflammatory cytokines and reactive oxygen species (ROS). Both microglial and astroglial cells, via a host of different mechanisms, contribute to pro-inflammatory states and ROS generation in the brain. Hence, it becomes essential to understand the impact of Ang II and neuroinflammatory mediators on the impairment of cardioregulatory centers in the brain, and to investigate the role of glia in Ang II-mediated sympathoexcitation. Understanding the mechanisms leading to an elevation in neuroinflammatory states, and the possible ways of counteracting it, could aid in devising better therapeutic strategies for the treatment of cardiovascular diseases and hypertension. This review primarily focuses on the molecular aspects of hypertension from a neuroinflammatory standpoint within brainstem cardiovascular centers.
DOI
10.1016/j.autneu.2018.01.002
Volume
210
First Page
10
Last Page
17
Disciplines
Medicine and Health Sciences | Pharmacy and Pharmaceutical Sciences
NSUWorks Citation
Haspula, Dhanush and Clark, Michelle A., "Neuroinflammation and Sympathetic Overactivity: Mechanisms and Implications in Hypertension" (2018). Faculty Articles. 301.
https://nsuworks.nova.edu/hpd_corx_facarticles/301
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