scholarly journals Regulation of the sympathetic nervous system by nitric oxide and oxidative stress in the rostral ventrolateral medulla: 2012 Academic Conference Award from the Japanese Society of Hypertension

2013 ◽  
Vol 36 (10) ◽  
pp. 845-851 ◽  
Author(s):  
Takuya Kishi
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Japanese Society ◽  
Rostral Ventrolateral Medulla ◽  
Ventrolateral Medulla ◽  
Academic Conference ◽  
Sympathetic Nervous ◽  
And Oxidative Stress

Cardiac autonomic function in acutely nitric oxide deficient hypertensive rats: role of the sympathetic nervous system and oxidative stress

2011 ◽  
Vol 89 (12) ◽  
pp. 865-874 ◽  
Author(s):  
Meenakshi Chaswal ◽  
Shobha Das ◽  
Jagdish Prasad ◽  
Anju Katyal ◽  
Mohammad Fahim
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
High Frequency ◽  
Spectral Power ◽  
Pressor Response ◽  
Sympathetic Nervous ◽  
And Oxidative Stress

We evaluated the role of the sympathetic nervous system and oxidative stress in hemodynamic and autonomic control after acute inhibition of the synthesis of nitric oxide, using intravenous (i.v.) injection of 30 mg·kg–1 NG-nitro-l-arginine methyl ester (L-NAME) in adult Wistar rats. Baroreflex sensitivity (BRS) and heart rate variability (HRV) were measured as indices of cardiac autonomic control, before and after L-NAME treatment in rats with intact autonomic innervation, and in rats with chemical sympathectomy by 6-hydroxydopamine. Serum malondialdehyde (MDA) was measured as a marker of oxidative stress. In control rats, L-NAME treatment resulted in a significant rise in blood pressure, augmentation of BRS, and enhanced serum MDA. HRV showed an attenuation of total spectral power and high frequency spectral power, along with a rise of the low to high frequency ratio (LF:HF). Administration of L-NAME produced a pressor response even in sympathectomised rats, but augmented BRS was not observed, and the high frequency spectral power showed an increase, in addition to a significant decline of LF:HF and serum MDA. We therefore conclude that even though pressor response was unaffected, reversal of cardiac autonomic responses and decline in oxidative stress following sympathectomy in L-NAME-treated rats reflects a significant role for sympathetic innervation in acute L-NAME-induced hypertension.

scholarly journals Physical (in)activity-dependent alterations at the rostral ventrolateral medulla: influence on sympathetic nervous system regulation

2010 ◽  
Vol 298 (6) ◽  
pp. R1468-R1474 ◽  
Author(s):  
Patrick J. Mueller
Keyword(s):  
Physical Activity ◽  
Cardiovascular Disease ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Rostral Ventrolateral Medulla ◽  
Ventrolateral Medulla ◽  
Organ Systems ◽  
Sympathetic Nervous ◽  
Activity Dependent ◽  
The Brain

A sedentary lifestyle is a major risk factor for cardiovascular disease, and rates of inactivity and cardiovascular disease are highly prevalent in our society. Cardiovascular disease is often associated with overactivity of the sympathetic nervous system, which has both direct and indirect effects on multiple organ systems. Although it has been known for some time that exercise positively affects the brain in terms of memory and cognition, only recently have changes in how the brain regulates the cardiovascular system been examined in terms of physical activity and inactivity. This brief review will discuss the evidence for physical activity-dependent neuroplasticity related to control of sympathetic outflow. It will focus particularly on recent studies from our laboratory and others that have examined changes that occur in the rostral ventrolateral medulla (RVLM), considered one of the primary brain regions involved in the regulation and generation of sympathetic nervous system activity.

Imbalance of central nitric oxide and reactive oxygen species in the regulation of sympathetic activity and neural mechanisms of hypertension

2011 ◽  
Vol 300 (4) ◽  
pp. R818-R826 ◽  
Author(s):  
Yoshitaka Hirooka ◽  
Takuya Kishi ◽  
Koji Sakai ◽  
Akira Takeshita ◽  
Kenji Sunagawa
Keyword(s):  
Nitric Oxide ◽  
Reactive Oxygen Species ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Brain Stem ◽  
Intracellular Signaling ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Sympathetic Nervous ◽  
The Brain

Nitric oxide (NO) and reactive oxygen species (ROS) play important roles in blood pressure regulation via the modulation of the autonomic nervous system, particularly in the central nervous system (CNS). In general, accumulating evidence suggests that NO inhibits, but ROS activates, the sympathetic nervous system. NO and ROS, however, interact with each other. Our consecutive studies and those of others strongly indicate that an imbalance between NO bioavailability and ROS generation in the CNS, including the brain stem, activates the sympathetic nervous system, and this mechanism is involved in the pathogenesis of neurogenic aspects of hypertension. In this review, we focus on the role of NO and ROS in the regulation of the sympathetic nervous system within the brain stem and subsequent cardiovascular control. Multiple mechanisms are proposed, including modulation of neurotransmitter release, inhibition of receptors, and alterations of intracellular signaling pathways. Together, the evidence indicates that an imbalance of NO and ROS in the CNS plays a pivotal role in the pathogenesis of hypertension.

scholarly journals Sympathetic Nervous System Control of Carbon Tetrachloride-Induced Oxidative Stress in Liver throughα-Adrenergic Signaling

2016 ◽  
Vol 2016 ◽  
pp. 1-11 ◽  
Author(s):  
Jung-Chun Lin ◽  
Yi-Jen Peng ◽  
Shih-Yu Wang ◽  
Mei-Ju Lai ◽  
Ton-Ho Young ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Nervous System ◽  
Carbon Tetrachloride ◽  
Sympathetic Nervous System ◽  
Nerve Fibers ◽  
Adrenergic Signaling ◽  
Adrenergic Antagonist ◽  
Sympathetic Nervous

In addition to being the primary organ involved in redox cycling, the liver is one of the most highly innervated tissues in mammals. The interaction between hepatocytes and sympathetic, parasympathetic, and peptidergic nerve fibers through a variety of neurotransmitters and signaling pathways is recognized as being important in the regulation of hepatocyte function, liver regeneration, and hepatic fibrosis. However, less is known regarding the role of the sympathetic nervous system (SNS) in modulating the hepatic response to oxidative stress. Our aim was to investigate the role of the SNS in healthy and oxidatively stressed liver parenchyma. Mice treated with 6-hydroxydopamine hydrobromide were used to realize chemical sympathectomy. Carbon tetrachloride (CCl4) injection was used to induce oxidative liver injury. Sympathectomized animals were protected from CCl4induced hepatic lipid peroxidation-mediated cytotoxicity and genotoxicity as assessed by 4-hydroxy-2-nonenal levels, morphological features of cell damage, and DNA oxidative damage. Furthermore, sympathectomy modulated hepatic inflammatory response induced by CCl4-mediated lipid peroxidation. CCl4induced lipid peroxidation and hepatotoxicity were suppressed by administration of anα-adrenergic antagonist. We conclude that the SNS provides a permissive microenvironment for hepatic oxidative stress indicating the possibility that targeting the hepaticα-adrenergic signaling could be a viable strategy for improving outcomes in patients with acute hepatic injury.

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