Evidence for descending tonic inhibition specifically affecting sympathetic pathways to the kidney in rats.

Hayes, Kristen; Yardley, Christopher; Weaver, Lynne C.

doi:10.1113/jphysiol.1991.sp018470

Cited by 16 publications

(8 citation statements)

References 29 publications

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“…With regard to the sympathetic premotor nuclei, the critical role of the RVLM in the tonic and phasic control of RSNA has been clearly demonstrated in several species 16 . For example, bilateral inhibition of RVLM neurons causes virtually complete abolition of RSNA 17,18 . Similarly, the increase in RSNA reflexly evoked by activation of somatic nociceptive afferent fibres or peripheral chemoreceptors is abolished by blockade of glutamate receptors in the RVLM 16 .…”

Section: Overview Of the Organization Of Central Pathways Controllingmentioning

confidence: 99%

Long‐term Regulation of Arterial Blood Pressure by Hypothalamic Nuclei: Some Critical Questions

Dampney

Horiuchi

Killinger

et al. 2005

Clin Exp Pharma Physio

178

140

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1. The long-term level of arterial pressure is dependent on the relationship between arterial pressure and the urinary output of salt and water, which, in turn, is affected by a number of factors, including renal sympathetic nerve activity (RSNA). In the present brief review, we consider the mechanisms within the brain that can influence RSNA, focusing particularly on hypothalamic mechanisms. 2. The paraventricular nucleus (PVN) in the hypothalamus has major direct and indirect connections with the sympathetic outflow and there is now considerable evidence that tonic activation of the PVN sympathetic pathway contributes to the sustained increased level of RSNA that occurs in conditions such as heart failure and neurogenic hypertension. The tonic activity of PVN sympathetic neurons, in turn, depends upon the balance of excitatory and inhibitory inputs. A number of neurotransmitters and neuromodulators are involved in these tonic excitatory and inhibitory effects, including glutamate, GABA, angiotensin II and nitric oxide. 3. The dorsomedial hypothalamic nucleus (DMH) also exerts a powerful influence over sympathetic activity, including RSNA, via synapses with sympathetic nuclei in the medulla and, possibly, also other brainstem regions. The DMH sympathetic pathway is an important component of the phasic sympathoexcitatory responses associated with acute stress, but there is no evidence that it is an important component of the central pathways that produce long-term changes in arterial pressure. Nevertheless, it is possible that repeated episodic activation of this pathway could lead to vascular hypertrophy and, thus, sustained changes in vascular resistance and arterial pressure. 4. Recent studies have reactivated the old debate concerning the possible role of the baroreceptor reflex in the long-term regulation of sympathetic activity. Therefore, central resetting of the baroreceptor-sympathetic reflex may be an important component of the mechanisms causing sustained changes in RSNA. However, little is known about the cellular mechanisms that could cause such resetting.

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Section: Overview Of the Organization Of Central Pathways Controllingmentioning

confidence: 99%

Long‐term Regulation of Arterial Blood Pressure by Hypothalamic Nuclei: Some Critical Questions

Dampney

Horiuchi

Killinger

et al. 2005

Clin Exp Pharma Physio

178

140

View full text Add to dashboard Cite

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“…21 In this context, it has been reported that most spinal cord reflexes appear to be inhibited by supraspinal centers. 22 It is tempting to speculate that when the autonomic nervous system is challenged, as during orthostatic stress, partial loss of this complex regulation, as occurs in tetraplegics, might allow a greater expression of positive feedback mechanisms than could be fully integrated at the spinal level. 12,22 Removal of supraspinal inhibition during stress would correspond to the observation that nonbaroreflex sequences increased in response to HUT in tetraplegics.…”

Section: Legramante Et Al Neural Feedback Regulating Circulation In Hmentioning

confidence: 99%

“…22 It is tempting to speculate that when the autonomic nervous system is challenged, as during orthostatic stress, partial loss of this complex regulation, as occurs in tetraplegics, might allow a greater expression of positive feedback mechanisms than could be fully integrated at the spinal level. 12,22 Removal of supraspinal inhibition during stress would correspond to the observation that nonbaroreflex sequences increased in response to HUT in tetraplegics. This interpretation would fit well with the observation of a central neural occlusive interaction between simultaneous stimulations of sympathetic and parasympathetic cardiac afferents that limits opposing cardiovascular reflex responses.…”

Section: Legramante Et Al Neural Feedback Regulating Circulation In Hmentioning

confidence: 99%

Positive and Negative Feedback Mechanisms in the Neural Regulation of Cardiovascular Function in Healthy and Spinal Cord–Injured Humans

et al. 2001

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“…HPA/SNS responses are coordinated in the spinal cord via supraspinal projections and by afferent feedback from the periphery to sympathetic preganglionic neurons (SPNs) (Hayes et al, 1991;Taylor and Weaver, 1993). SPNs found throughout the thoracic spinal cord (T3-13; (Strack et al, 1989;Cano et al, 2001) influence immune function through post-ganglionic noradrenergic projections to spleen (Wan et al, 1993) and adrenal cortex (Bloom et al, 1988;Engeland, 1998).…”

Section: Introductionmentioning

confidence: 99%

Impaired antibody synthesis after spinal cord injury is level dependent and is due to sympathetic nervous system dysregulation

Lucin

Sanders

Jones

et al. 2007

Experimental Neurology

171

217

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Individuals with spinal cord injury (SCI) are highly susceptible to infection. This post-traumatic immune suppression is thought to occur via alterations in sympathetic nervous system (SNS) or hypothalamic-pituitary-adrenal (HPA) axis function. Normally, the HPA axis and SNS help coordinate proper immune function. After SCI, the HPA axis becomes activated and descending input to sympathetic preganglionic neurons (SPNs) is impaired. Because lymphoid organs are innervated by SPNs distributed throughout the thoracolumbar spinal cord, we predicted leveldependent immune suppression after SCI due to activation of the HPA axis and loss of descending input to SPNs. We tested this hypothesis by measuring indices of HPA (circulating corticosterone; CORT) and SNS function (norepinephrine (NE) in spleen) as well as antigen-specific antibody synthesis against an exogenous non-self protein following high or low level SCI. Using a midthoracic (T9) spinal contusion injury model, we found that CORT was elevated after SCI with aberrant patterns of diurnal CORT synthesis evident through at least the first 24 hours post-injury. However, splenic NE and antibody synthesis were similar to uninjured controls. Injury severity did not change these parameters. Indeed, CORT, NE and antibody synthesis were similar after T9 contusion or transection SCI. In contrast, high level SCI (T3) caused sustained increases in CORT and splenic NE along with impaired antibody synthesis and elevated splenocyte apoptosis. The immunosuppressive effects of T3 SCI were caused by NE acting at β2-adrenergic receptors (β2AR) and could be reversed using β2AR blockers. Interestingly, impaired antibody after T3 SCI could be Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. NIH Public Access NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript mimicked after T9 SCI with a β2AR agonist. These data illustrate the immunosuppressive effects of the SNS after high-level SCI and indicate that immune deficits may be overcome using β-blockers.

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Evidence for descending tonic inhibition specifically affecting sympathetic pathways to the kidney in rats.

Cited by 16 publications

References 29 publications

Long‐term Regulation of Arterial Blood Pressure by Hypothalamic Nuclei: Some Critical Questions

Long‐term Regulation of Arterial Blood Pressure by Hypothalamic Nuclei: Some Critical Questions

Positive and Negative Feedback Mechanisms in the Neural Regulation of Cardiovascular Function in Healthy and Spinal Cord–Injured Humans

Impaired antibody synthesis after spinal cord injury is level dependent and is due to sympathetic nervous system dysregulation

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