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Sympathetic regulation of vascular function in health and disease.

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TLDR
In humans large artery stiffness has been associated with increased sympathetic discharge, both in healthy subjects and in renal transplant recipients, and peripheral sympathetic discharge is also able to modulate wave reflection, which can interfere with autonomic regulation by impairing carotid baroreflex sensitivity.
Abstract
The sympathetic nervous system (SNS) is known to play a pivotal role in short- and long-term regulation of different functions of the cardiovascular system. In the past decades increasing evidence demonstrated that sympathetic neural control is involved not only in the vasomotor control of small resistance arteries but also in modulation of large artery function. Sympathetic activity and vascular function, both of which are key factors in the development and prognosis of cardiovascular events and disease, are linked at several levels. Evidence from experimental studies indicates that the SNS is critically influenced, at the central and also at the peripheral level, by the most relevant factors regulating vascular function, such as nitric oxide (NO), reactive oxygen species (ROS), endothelin (ET), the renin-angiotensin system. Additionally, there is indirect evidence of a reciprocal relationship between endothelial function and activity of the SNS. A number of cardiovascular risk factors and diseases are characterized both by increased sympathetic outflow and decreased endothelial function. In healthy subjects, muscle sympathetic nerve activity (MSNA) appears to be related to surrogate markers of endothelial function, and an acute increase in sympathetic activity has been associated with a decrease in endothelial function in healthy subjects. However, direct evidence of a cause-effect relationship from human studies is scanty. In humans large artery stiffness has been associated with increased sympathetic discharge, both in healthy subjects and in renal transplant recipients. Peripheral sympathetic discharge is also able to modulate wave reflection. On the other hand, large artery stiffness can interfere with autonomic regulation by impairing carotid baroreflex sensitivity.

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Increased Reactive Oxygen Species in Rostral Ventrolateral Medulla Contribute to Neural Mechanisms of Hypertension in Stroke-Prone Spontaneously Hypertensive Rats

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References
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Journal ArticleDOI

Expert consensus document on arterial stiffness: methodological issues and clinical applications

TL;DR: This paper summarizes the proceedings of several meetings of the European Network for Non-invasive Investigation of Large Arteries and is aimed at providing an updated and practical overview of the most relevant methodological aspects and clinical applications in this area.
Journal Article

Expert consensus document on arterial stiffness : methodological issues and clinical applications. Commentary

TL;DR: In this paper, the authors summarized the proceedings of several meetings of the European Network for Non-invasive Investigation of Large Arteries and aimed at providing an updated and practical overview of the most relevant methodological aspects and clinical applications in this area.
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Prediction of cardiovascular events and all-cause mortality with arterial stiffness: a systematic review and meta-analysis.

TL;DR: Aortic stiffness expressed as aortic PWV is a strong predictor of future CV events and all-cause mortality and the predictive ability of arterial stiffness is higher in subjects with a higher baseline CV risk.
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Localization of nitric oxide synthase indicating a neural role for nitric oxide

TL;DR: It is demonstrated that NO synthase in the brain to be exclusively associated with discrete neuronal populations, and prominent neural localizations provided the first conclusive evidence for a strong association of NO with neurons.
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Angiotensin II stimulates NADH and NADPH oxidase activity in cultured vascular smooth muscle cells.

TL;DR: The ability of Ang II to stimulate superoxide anion formation is examined and the identity of the oxidases responsible for its production is investigated to suggest that Ang II specifically activates enzyme systems that promote superoxide generation and raise the possibility that these pathways function as second messengers for long-term responses, such as hypertrophy or hyperplasia.
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