Integration of renal sensory afferents at the level of the paraventricular nucleus dictating sympathetic outflow

Zheng, Hong; Patel, Kaushik P.

doi:10.1016/j.autneu.2016.08.008

Cited by 39 publications

(24 citation statements)

References 103 publications

(123 reference statements)

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“…Moreover, these vagus afferents target the nucleus of the solitary tract in the brain, an area that is important for regulation of autonomic function in the periphery 97 . Electrophysiological data showing that neurons in the hypothalamus are excited after stimulation of renal sensory afferents through a pathway that may involve areas of the medulla, suggest that renal sensory afferent information might also be integrated in the hypothalamus 98 .…”

Section: Neural Circuits In the Kidneymentioning

confidence: 99%

Targeting neural reflex circuits in immunity to treat kidney disease

2017

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Neural pathways regulate immunity and inflammation via the inflammatory reflex and specific molecular targets can be modulated by stimulating neurons. Neuroimmunomodulation by nonpharmacological methods is emerging as a novel therapeutic strategy for inflammatory diseases, including kidney diseases and hypertension. Electrical stimulation of vagus neurons or treatment with pulsed ultrasound activates the cholinergic anti-inflammatory pathway (CAP) and protects mice from acute kidney injury (AKI). Direct innervation of the kidney, by afferent and efferent neurons, might have a role in modulating and responding to inflammation in various diseases, either locally or by providing feedback to regions of the central nervous system that are important in the inflammatory reflex pathway. Increased sympathetic drive to the kidney has a role in the pathogenesis of hypertension, and selective modulation of neuroimmune interactions in the kidney could potentially be more effective for lowering blood pressure and treating inflammatory kidney diseases than renal denervation. Use of optogenetic tools for selective stimulation of specific neurons has enabled the identification of neural circuits in the brain that modulate kidney function via activation of the CAP. In this Review we discuss evidence for a role of neural circuits in the control of renal inflammation as well as the therapeutic potential of targeting these circuits in the settings of AKI, kidney fibrosis and hypertension.

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Section: Neural Circuits In the Kidneymentioning

confidence: 99%

Targeting neural reflex circuits in immunity to treat kidney disease

2017

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“…On the other hand, experimental evidence shows that the afferent signaling resulting from renal injury increases efferent renal sympathetic activity leading to hypertension 30 . The enhanced or altered afferent renal input to the paraventricular nucleus in disease conditions may be involved in producing elevated sympathetic nerve activity 31 . In addition, evidence indicates that functional ablation of renal afferent fibers does not affect the regulation of arterial pressure in normal conditions but may play a role in the development of salt-sensitive hypertension 32 .…”

Section: Renal Sympathetic Innervation: Physiological Role Of Efferenmentioning

confidence: 99%

Renal sympathetic denervation for resistant hypertension: where do we stand after more than a decade

et al. 2020

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Despite the current availability of safe and efficient drugs for treating hypertension, a substantial number of patients are drug-resistant hypertensives. Aiming this condition, a relatively new approach named catheter-based renal denervation was developed. We have now a clinically relevant time window to review the efficacy of renal denervation for treating this form of hypertension. This short review addresses the physiological contribution of renal sympathetic nerves for blood pressure control and discusses the pros and cons of renal denervation procedure for the treatment of resistant hypertension.

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“…The paraventricular nucleus (PVN) of the hypothalamus is an important forebrain center that integrates and responds to a variety of neural and humoral signals regulating sympathetic drive and extracellular fluid volume status ( Badoer, 2010 ; Zheng and Patel, 2017 ). Activation of the PVN has been shown to increase sympathetic nerve activity and blood pressure in rats exposed to CIH ( Knight et al, 2011 ; Sharpe et al, 2013 ).…”

Section: Introductionmentioning

confidence: 99%

Elevated Oxidative Stress and Inflammation in Hypothalamic Paraventricular Nucleus Are Associated With Sympathetic Excitation and Hypertension in Rats Exposed to Chronic Intermittent Hypoxia

Yan-li

Gua

et al. 2018

Front. Physiol.

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Obstructive sleep apnea (OSA), characterized by recurrent collapse of the upper airway during sleep leading to chronic intermittent hypoxia (CIH), is an independent risk factor for hypertension. Sympathetic excitation has been shown to play a major role in the pathogenesis of OSA-associated hypertension. Accumulating evidence indicates that oxidative stress and inflammation in the hypothalamic paraventricular nucleus (PVN), a critical cardiovascular and autonomic center, mediate sympathetic excitation in many cardiovascular diseases. Here we tested the hypothesis that CIH elevates oxidative stress and inflammation in the PVN, which might be associated with sympathetic excitation and increased blood pressure in a rat model of CIH that mimics the oxygen profile in patients with OSA. Sprague-Dawley rats were pretreated with intracerebroventricular (ICV) infusion of vehicle or superoxide scavenger tempol, and then exposed to control or CIH for 7 days. Compared with control+vehicle rats, CIH+vehicle rats exhibited increased blood pressure, and increased sympathetic drive as indicated by the blood pressure response to ganglionic blockade and plasma norepinephrine levels. Pretreatment with ICV tempol prevented CIH-induced increases in blood pressure and sympathetic drive. Molecular studies revealed that expression of NAD(P)H oxidase subunits, production of reactive oxygen species, expression of proinflammatory cytokines and neuronal excitation in the PVN were elevated in CIH+vehicle rats, compared with control+vehicle rats, but were normalized or reduced in CIH rat pretreated with ICV tempol. Notably, CIH+vehicle rats also had increased systemic oxidative stress and inflammation, which were not altered by ICV tempol. The results suggest that CIH induces elevated oxidative stress and inflammation in the PVN, which lead to PVN neuronal excitation and are associated with sympathetic excitation and increased blood pressure. Central oxidative stress and inflammation may be novel targets for the prevention and treatment of hypertension in patients with OSA.

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Integration of renal sensory afferents at the level of the paraventricular nucleus dictating sympathetic outflow

Cited by 39 publications

References 103 publications

Targeting neural reflex circuits in immunity to treat kidney disease

Targeting neural reflex circuits in immunity to treat kidney disease

Renal sympathetic denervation for resistant hypertension: where do we stand after more than a decade

Elevated Oxidative Stress and Inflammation in Hypothalamic Paraventricular Nucleus Are Associated With Sympathetic Excitation and Hypertension in Rats Exposed to Chronic Intermittent Hypoxia

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