Differential activation of adrenal, renal, and lumbar sympathetic nerves following stimulation of the rostral ventrolateral medulla of the rat

Mueller, Patrick; Mischel, Nicholas; Scislo, Tadeusz J.

doi:10.1152/ajpregu.00713.2010

Cited by 39 publications

(62 citation statements)

References 78 publications

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“…A fundamental regulatory strategy of the SNS involves selectively controlling the level of activity in nerves innervating different targets (Hirai et al, 1995; Morrison, 2001; Miki and Yoshimoto, 2010; Mueller et al, 2011). The results of previous studies (Oku et al, 1996; Xu et al, 1998) demonstrate that Dex administration produces renal sympathoinhibition.…”

Section: Discussionmentioning

confidence: 99%

Dexmedetomidine and regulation of splenic sympathetic nerve discharge

Kenney¹,

Larsen²,

McMurphy³

et al. 2014

Autonomic Neuroscience

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Recent lines of inquiry indicate sedatives can influence the immune system, leading to the concept of sedative-induced immunomodulation. It has been hypothesized that sedatives may alter immune responses by modulating the sympathetic nervous system, however, little information is known regarding the effects of sedatives on regulation of splenic sympathetic nerve discharge (SND), a significant omission based on the functional role that changes in splenic SND exert on splenic cytokine gene expression. The present investigation determined the effect of systemic Dexmedetomidine (Dex) administration on the level of directly-recorded splenic SND and tested the hypothesis that the intravenous administration of Dex would inhibit splenic SND in anesthetized rats. The present results demonstrate for the first time that intravenous Dex administration significantly reduces splenic sympathetic nerve outflow in baroreceptor-intact and sinoaortic-denervated rats, indicating that Dex administration alters the central regulation of splenic SND. The present results provide new information regarding the effect of a centrally-acting alpha2-adrenergic agonist on the level of sympathetic nerve outflow to a secondary lymphoid organ that plays a critical role in peripheral immune responses.

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Section: Discussionmentioning

confidence: 99%

Dexmedetomidine and regulation of splenic sympathetic nerve discharge

Kenney¹,

Larsen²,

McMurphy³

et al. 2014

Autonomic Neuroscience

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“…Since generalized activation of the RVLM affects multiple sympathetic outputs (45,52), it is likely that similar blood pressure responses are due to additional differences between sedentary and active animals not directly addressed in this study. For example, enhanced vasoconstriction in sedentary animals may be offset by relatively reduced myocardial contractility responses produced during sympathetic stimulation (3,67).…”

Section: Discussionmentioning

confidence: 99%

“…In fact, we argued recently that comparing voltages across functionally different nerves may not be physiologically relevant (52). However, in the present study we chose to report our SSNA data in volts, as has been done by previous investigators (25,26,38,40).…”

Section: Technical Considerationsmentioning

confidence: 99%

“…These spinally projecting RVLM neurons are regulated by the major inhibitory and excitatory neurotransmitters GABA and glutamate, respectively (19,43). Microinjection of glutamate and glutamate receptor agonists into the RVLM results in large increases in sympathetic nerve activity and blood pressure (1, 18,39,52,60,62). Our laboratory and others have shown that sedentary vs. active rats exhibit greater indexes of sympathoexcitation when RVLM neurons are activated with glutamate (41, 50).…”

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confidence: 99%

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(In)activity-dependent alterations in resting and reflex control of splanchnic sympathetic nerve activity

Mischel

Mueller

2011

Journal of Applied Physiology

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Mischel NA, Mueller PJ. (In)activity-dependent alterations in resting and reflex control of splanchnic sympathetic nerve activity. J Appl Physiol 111: 1854 -1862. First published October 6, 2011 doi:10.1152/japplphysiol.00961.2011The negative effects of sympathetic overactivity on long-term cardiovascular health are becoming increasingly clear. Moreover, recent work done in animal models of cardiovascular disease suggests that sympathetic tone to the splanchnic vasculature may play an important role in the development and maintenance of these disease states. Work from our laboratory and others led us to hypothesize that a lack of chronic physical activity increases resting and reflex-mediated splanchnic sympathetic nerve activity, possibly through changes occurring in a key brain stem center involved in sympathetic regulation, the rostral ventrolateral medulla (RVLM). To address this hypothesis, we recorded mean arterial pressure (MAP) and splanchnic sympathetic nerve activity (SSNA) in a group of active and sedentary animals that had been housed for 10 -13 wk with or without running wheels, respectively. In experiments performed under Inactin anesthesia, we tested responses to RVLM microinjections of glutamate, responses to baroreceptor unloading, and vascular reactivity, the latter of which was performed under conditions of autonomic blockade. Sedentary animals exhibited enhanced resting SSNA and MAP, augmented increases in SSNA to RVLM activation and baroreceptor unloading, and enhanced vascular reactivity to ␣ 1-receptor mediated vasoconstriction. Our results suggest that a sedentary lifestyle increases the risk of cardiovascular disease by augmenting resting and reflex-mediated sympathetic output to the splanchnic circulation and also by increasing vascular sensitivity to adrenergic stimulation. We speculate that regular physical exercise offsets or reverses the progression of these disease processes via similar or disparate mechanisms and warrant further examination into physical (in)activity-induced sympathetic nervous system plasticity. sympathetic nervous system; sedentary lifestyle; blood pressure CARDIOVASCULAR DISEASE is currently the leading cause of death in the United States and has an economic impact in the hundreds of billions of dollars (35,58). One of the primary risk factors for cardiovascular disease is a lack of regular exercise (35). The detrimental effects of a sedentary lifestyle on cardiovascular health have been studied and documented for over 50 yr (2,11,48). However, only recently have many conditions linked to physical inactivity, such as the metabolic syndrome, heart failure, and hypertension, been associated with overactivity of the sympathetic nervous system (7,13,14,22,29,63,68). Since sympathetic overactivity can have deleterious effects on the cardiovascular system both directly and indirectly (16,17), it is important to study the mechanisms by which physical inactivity can raise sympathetic output and negatively impact the cardiovascular system. Sympathetic activity is gener...

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“…The C1 neurons with spinal projections may consist of several subsets that differentially control sympathetic tone to various cardiovascular organs or vascular beds (McAllen et al 1997; Mueller et al 2011). However, stimulation of the C1 neurons also causes arousal, sighs, stimulates breathing and activates vagal efferents, thus demonstrating that these neurons are involved in more than just cardiovascular control (Abbott et al 2014a; Holloway et al 2013; Burke et al 2014; Guyenet et al 2013).…”

Section: Introductionmentioning

confidence: 99%

Afferent and efferent connections of C1 cells with spinal cord or hypothalamic projections in mice

2015

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The axonal projections and synaptic input of the C1 adrenergic neurons of the rostral ventrolateral medulla, (VLM) were examined using transgenic dopamine-beta hydroxylase (DβH) Cre mice and modified rabies virus. Cre-dependent viral vectors expressing TVA (receptor for envelopeA) and rabies glycoprotein were injected into the left VLM. EnvelopeA-pseudotyped rabies-EGFP glycoprotein-deficient virus (rabies-EGFP) was injected 4–6 weeks later in either thoracic spinal cord (SC) or hypothalamus. TVA immunoreactivity was detected almost exclusively (95%) in VLM C1 neurons. In mice with SC injections of rabies-EGFP, starter cells (expressing TVA + EGFP) were found at the rostral end of the VLM; in mice with hypothalamic injections starter C1 cells were located more caudally. C1 neurons innervating SC or hypothalamus had other terminal fields in common (e.g., dorsal vagal complex, locus coeruleus, raphe pallidus and periaqueductal gray matter). Putative inputs to C1 cells with SC or hypothalamic projections originated from the same brain regions, especially the lower brainstem reticular core from spinomedullary border to rostral pons. Putative input neurons to C1 cells were also observed in the nucleus of the solitary tract, caudal VLM, caudal spinal trigeminal nucleus, cerebellum, periaqueductal gray matter and inferior and superior colliculi. In sum, regardless of whether they innervate SC or hypothalamus, VLM C1 neurons receive input from the same general brain regions. One interpretation is that many types of somatic or internal stimuli recruit these neurons en bloc to produce a stereotyped acute stress response with sympathetic, parasympathetic, vigilance and neuroendocrine components.

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Differential activation of adrenal, renal, and lumbar sympathetic nerves following stimulation of the rostral ventrolateral medulla of the rat

Cited by 39 publications

References 78 publications

Dexmedetomidine and regulation of splenic sympathetic nerve discharge

Dexmedetomidine and regulation of splenic sympathetic nerve discharge

(In)activity-dependent alterations in resting and reflex control of splanchnic sympathetic nerve activity

Afferent and efferent connections of C1 cells with spinal cord or hypothalamic projections in mice

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