Altered frequency responses of sympathetic nerve  discharge bursts after IL-1β and mild hypothermia

Kenney, Michael J.; Blecha, Frank; Fels, Richard J.; Morgan, Donald A.

doi:10.1152/japplphysiol.01250.2001

Cited by 5 publications

(4 citation statements)

References 47 publications

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“…Moreover, Niijima et al (210) reported that intravenous IL-1β increased adrenal and splenic SND, but produced only transient increases followed by sustained reductions in renal SND in urethane-anesthetized rats. Third, the frequency-domain coupling of SND bursts can be influenced by IL-1β alone and in response to combined IL-1β and mild hypothermia (150), suggesting an additional mechanism via which IL-1β can influence sympathetic nerve outflow. Fourth, IL-1β can modulate responses to other physiological interventions.…”

Section: Cytokines Immune System Mediators and Autonomic Nerve Respomentioning

confidence: 99%

“…However, recent lines of inquiry have expanded the functional repertoire of the ANS by establishing an essential role for this system in regulating, integrating, and orchestrating processes between diverse physiological systems (49, 51, 71, 96, 112). Specifically, the results of many studies (71, 96, 97, 120, 121, 134, 135, 136, 150, 152, 181, 200, 256, 281, 296, 297, 298) have established a critical role for the ANS in mediating interactions between the nervous and immune systems, two important adaptive systems that were originally considered to function independently of each other. The physiology of ANS function and regulation involves numerous complex, dynamic, and integrated steps (e.g., neural outflow, transmitter synthesis, release and degradation, ganglionic regulation, receptor-mediated effects), many of which are likely involved in mediating neural-immune interactions.…”

Section: Introductionmentioning

confidence: 99%

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Autonomic Nervous System and Immune System Interactions

Kenney

Ganta

2014

Comprehensive Physiology

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289

218

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The present review assesses the current state of literature defining integrative autonomic-immune physiological processing, focusing on studies that have employed electrophysiological, pharmacological, molecular biological and central nervous system experimental approaches. Central autonomic neural networks are informed of peripheral immune status via numerous communicating pathways, including neural and non-neural. Cytokines and other immune factors affect the level of activity and responsivity of discharges in sympathetic and parasympathetic nerves innervating diverse targets. Multiple levels of the neuraxis contribute to cytokine-induced changes in efferent parasympathetic and sympathetic nerve outflows, leading to modulation of peripheral immune responses. The functionality of local sympathoimmune interactions depends on the microenvironment created by diverse signaling mechanisms involving integration between sympathetic nervous system neurotransmitters and neuromodulators; specific adrenergic receptors; and the presence or absence of immune cells, cytokines and bacteria. Functional mechanisms contributing to the cholinergic anti-inflammatory pathway likely involve novel cholinergic-adrenergic interactions at peripheral sites, including autonomic ganglion and lymphoid targets. Immune cells express adrenergic and nicotinic receptors. Neurotransmitters released by sympathetic and parasympathetic nerve endings bind to their respective receptors located on the surface of immune cells and initiate immune-modulatory responses. Both sympathetic and parasympathetic arms of the autonomic nervous system are instrumental in orchestrating neuroimmune processes, although additional studies are required to understand dynamic and complex adrenergic-cholinergic interactions. Further understanding of regulatory mechanisms linking the sympathetic nervous, parasympathetic nervous, and immune systems is critical for understanding relationships between chronic disease development and immune-associated changes in autonomic nervous system function.

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Section: Cytokines Immune System Mediators and Autonomic Nerve Respomentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Autonomic Nervous System and Immune System Interactions

Kenney

Ganta

2014

Comprehensive Physiology

Self Cite

289

218

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“…Several studies suggest a relationship between activation of IL-1R and autonomic nervous system activity (see Graphical Abstract). Intravenous infusion of IL-1β in conscious rats 20 increased renal nerve activity and arterial pressure and spinal cord transection at C1 before infusion abolished sympathoexcitation, 21 suggesting a peripheral location of action involving activation of afferent pathways that modulate sympathetic activity.…”

Section: Potential Mechanisms Mediating the Interaction Of The Il-1r ...mentioning

confidence: 99%

IL-1R Mediated Activation of Renal Sensory Nerves in DOCA-Salt Hypertension

Baumann,

Van Helden,

Evans

et al. 2024

Hypertension

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BACKGROUND: Clinical trials of renal denervation for the treatment of hypertension have shown a variety of off-target improvements in conditions associated with sympathetic overactivity. This may be due to the ablation of sympathoexcitatory afferent renal nerves, which are overactive under conditions of renal inflammation. Renal IL (interleukin)-1β is elevated in the deoxycorticosterone acetate-salt model of hypertension, and its activity may be responsible for the elevation in afferent renal nerve activity and arterial pressure. METHODS: Continuous blood pressure recording of deoxycorticosterone acetate-salt mice with IL-1R (IL-1 receptor) knockout or antagonism was used individually and combined with afferent renal denervation (ARDN) to assess mechanistic overlap. Protein quantification and histological analysis of kidneys were performed to characterize renal inflammation. RESULTS: ARDN attenuated deoxycorticosterone acetate-salt hypertension (−20±2-Δmm Hg mean arterial pressure [MAP] relative to control at study end) to a similar degree as total renal denervation (−21±2-Δmm Hg MAP), IL-1R knockout (−16±4-Δmm Hg MAP), or IL-1R antagonism (−20±3-Δmm Hg MAP). The combination of ARDN with knockout (−18±2-Δmm Hg MAP) or antagonism (−19±4-Δmm Hg MAP) did not attenuate hypertension any further than ARDN alone. IL-1R antagonism was found to have an acute depressor effect (−15±3-Δmm Hg MAP, day 10) in animals with intact renal nerves but not those with ARDN. CONCLUSIONS: These findings suggest that IL-1R signaling is partially responsible for the elevated afferent renal nerve activity, which stimulates central sympathetic outflow to drive deoxycorticosterone acetate-salt hypertension.

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“…Studies in experimental rats have shaped the contemporary understanding of central mechanisms regulating basal SND and the role of central neural circuits in mediating changes in SND responses to acute stress. For example, it is well-established that central sympathetic neural circuits in experimental rats are capable of producing heterogeneous SND response profiles to numerous interventions, including directionally opposite changes in the level of activity in sympathetic nerves innervating different targets and selectivity in the frequency-domain characteristics of discharge bursts in different sympathetic nerves (Kenney, 1994; Kenney et al, 2002; Kenney et al, 1999; Morrison, 2001; Ramchandra et al, 2006; Weiss et al, 1996). Moreover, it is well-recognized that multiple levels of the neuraxis contribute to regulation of efferent SND and that various pathophysiological conditions can alter the central regulation of SND in experimental animals (Dampney, 1994; Dampney et al, 2003; Guyenet, 2006; Loewy, 1990; Strack et al, 1989; Sun, 1995).…”

Section: Translational Physiology and Snd Recordingsmentioning

confidence: 99%

Translational physiology and SND recordings in humans and rats: A glimpse of the recent past with an eye on the future

Kenney

Mosher

2013

Autonomic Neuroscience

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The sympathetic nervous system (SNS) plays an important role in cardiovascular function, and based on the critical mechanistic relationship between altered sympathetic neural mechanisms and cardiovascular disease, it is important that the autonomic research community identify deficiencies in the translational exchange of information and strive for a more thorough understanding of the translational significance of findings from studies involving sympathetic nerve discharge (SND) regulation in human and animal subjects. The present review assesses the state of the literature regarding studies that have used direct recordings of SND during the past three decades in humans and rats, focusing on; 1) identifying the number of studies reporting SND recordings in humans and rats, 2) briefly describing the translational exchange of SND regulation information from these studies, 3) contrasting the number of studies completed in anesthetized and conscious rats, and 4) assessing the prevalence of long-term SND recording studies in conscious rats. The majority of SND recordings in rats have been completed using anesthetized preparations, although a substantial number of studies have been completed in conscious rats. However, few studies have completed long-term (>5 days) SND recordings in freely-behaving rats, and even fewer studies have used experimental preparations that combine long-term nerve recordings with the capacity for completing central neural microinjections, or have been completed in animal models of cardiovascular disease. The wide-spread implementation of long-term SND recordings in rodent models of cardiovascular disease would be expected to enhance the translational exchange of clinically-relevant information between animals and humans.

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Altered frequency responses of sympathetic nerve discharge bursts after IL-1β and mild hypothermia

Cited by 5 publications

References 47 publications

Autonomic Nervous System and Immune System Interactions

Autonomic Nervous System and Immune System Interactions

IL-1R Mediated Activation of Renal Sensory Nerves in DOCA-Salt Hypertension

Translational physiology and SND recordings in humans and rats: A glimpse of the recent past with an eye on the future

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