scholarly journals Stimulation of skin sympathetic nerve discharge by central command. Differential control of sympathetic outflow to skin and skeletal muscle during static exercise.

1991 ◽  
Vol 69 (1) ◽  
pp. 228-238 ◽  
Author(s):  
S F Vissing ◽  
U Scherrer ◽  
R G Victor
Keyword(s):  
Skeletal Muscle ◽  
Sympathetic Nerve ◽  
Sympathetic Outflow ◽  
Central Command ◽  
Static Exercise ◽  
Differential Control ◽  
Stimulation Of ◽  
Nerve Discharge

Muscle reflex stimulates sympathetic postganglionic efferents innervating triceps surae muscles of cats

1996 ◽  
Vol 271 (1) ◽  
pp. H38-H43 ◽  
Author(s):  
J. M. Hill ◽  
C. M. Adreani ◽  
M. P. Kaufman
Keyword(s):  
Skeletal Muscle ◽  
Electrical Stimulation ◽  
Cardiovascular Function ◽  
Triceps Surae ◽  
Sympathetic Outflow ◽  
Central Command ◽  
Muscle Reflex ◽  
Triceps Surae Muscles ◽  
Nerve Recordings ◽  
Stimulation Of

Two neural mechanisms contribute to the cardiovascular responses to exercise. The first, central command, proposes a parallel activation of central locomotor and brain stem circuits controlling cardiovascular function. The second, the muscle reflex, proposes that contraction-activated group III and IV afferents increase cardiovascular function. In humans, whole nerve recordings of sympathetic discharge suggest that central command increases sympathetic outflow to skin but not to skeletal muscle and that the muscle reflex increases sympathetic outflow to skeletal muscle but not to skin. We therefore tested the hypothesis that the muscle reflex, but not central command, increases the discharge of single sympathetic postganglionic efferents innervating the triceps surae muscles of decerebrate unanesthetized cats. Central command was evoked by electrical stimulation of the mesencephalic locomotor region. The reflex was evoked by electrical stimulation of the tibial nerve, which in turn contracted the triceps surae muscles. Hexamethonium abolished spontaneous and evoked activity, verifying that the recordings were from sympathetic postganglionic fibers. The discharge of 13 efferents was increased by static contraction (from 0.6 +/- 0.2 to 1.0 +/- 0.3 imp/s; P < 0.05) but was not increased by central command (from 0.6 +/- 0.2 to 0.8 +/- 0.2 imp/s; P > 0.05). Nevertheless, the discharge of nine efferents, not increased by central command before alpha-adrenergic blockade (from 0.5 +/- 0.2 to 0.9 +/- 0.4 imp/s; P > 0.05), was increased after blockade (from 1.3 +/- 0.2 to 3.2 +/- 0.8 imp/s; P < 0.05). We conclude that the muscle reflex stimulates sympathetic postganglionic efferents innervating the vasculature of skeletal muscle. Furthermore, baroreceptors appear to buffer the central command-induced increases in the discharge of these efferents.

NMDA-mediated increase in renal sympathetic nerve discharge within the PVN: role of nitric oxide

2001 ◽  
Vol 281 (6) ◽  
pp. H2328-H2336 ◽  
Author(s):  
Yi-Fan Li ◽  
William G. Mayhan ◽  
Kaushik P. Patel
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Dependent Manner ◽  
Sympathetic Outflow ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic Nerve ◽  
Dose Dependent ◽  
Renal Sympathetic ◽  
Nerve Discharge

The paraventricular nucleus (PVN) of the hypothalamus is an important site of integration in the central nervous system for sympathetic outflow. Both glutamate and nitric oxide (NO) play an important role in the regulation of sympathetic nerve activity. The purpose of the present study was to examine the interaction of NO and glutamate within the PVN in the regulation of renal sympathetic nerve activity in rats. Renal sympathetic nerve discharge (RSND), arterial blood pressure (BP), and heart rate (HR) were measured in response to administration of N-methyl-d-aspartic acid (NMDA) and N G-monomethyl-l-arginine (l-NMMA) into the PVN. We found that microinjection of NMDA (25, 50, and 100 pmol) into the PVN increased RSND, BP, and HR in a dose-dependent manner, reaching 53 ± 9%, 19 ± 3 mmHg, and 32 ± 12 beats/min, respectively, at the highest dose. These responses were significantly enhanced by prior microinjection ofl-NMMA. On the other hand, inhibition of NO within the PVN by microinjection of l-NMMA also induced increases in RSND, BP, and HR in a dose-dependent manner, reaching 48 ± 6.5%, 11 ± 4 mmHg, and 55 ± 16 beats/min, respectively, at the highest dose. This sympathoexcitatory response was eliminated by prior microinjection of dl-2-amino-5-phosphonovaleric acid, an antagonist of the NMDA receptor. Furthermore, with the use of the push-pull technique, perfusion of glutamate (0.5 μmol) or NMDA (0.1 nmol) into the PVN induced an increase in NO release. In conclusion, our data indicate that NMDA receptors within the PVN mediate an excitatory effect on renal sympathetic nerve activity, arterial BP, and HR. NO in the PVN, which is released by activation of the NMDA receptor, also inhibits NMDA-mediated increases in sympathetic nerve activity. This negative feedback of NO on the glutamate system within the PVN may play an important role in maintaining the overall balance and tone of sympathetic outflow in normal and pathophysiological conditions known to have increased sympathetic tone.

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

2011 ◽  
Vol 300 (5) ◽  
pp. R1230-R1240 ◽  
Author(s):  
Patrick J. Mueller ◽  
Nicholas A. Mischel ◽  
Tadeusz J. Scislo
Keyword(s):  
Sympathetic Nerve ◽  
Chronic Conditions ◽  
Sympathetic Nerves ◽  
Rostral Ventrolateral Medulla ◽  
Ventrolateral Medulla ◽  
Differential Activation ◽  
Sympathetic Nervous ◽  
Percentage Basis ◽  
Differential Control ◽  
Stimulation Of

Under acute and chronic conditions, the sympathetic nervous system can be activated in a differential and even selective manner. Activation of the rostral ventrolateral medulla (RVLM) has been implicated in differential control of sympathetic outputs based on evidence primarily in the cat. Although several studies indicate that differential control of sympathetic outflow occurs in other species, only a few studies have addressed whether the RVLM is capable of producing varying patterns of sympathetic activation in the rat. Therefore, the purpose of the present study was to determine whether activation of the RVLM results in simultaneous and differential increases in preganglionic adrenal (pre-ASNA), renal (RSNA), and lumbar (LSNA) sympathetic nerve activities. In urethane-chloralose anesthetized rats, pre-ASNA, RSNA, and LSNA were recorded simultaneously in all animals. Microinjections of selected concentrations and volumes of glutamate increased pre-ASNA, RSNA, and LSNA concurrently and differentially. Pre-ASNA and RSNA (in most cases) exhibited greater increases compared with LSNA on a percentage basis. By varying the volume or location of the glutamate microinjections, we also identified individual examples of differential and selective activation of these nerves. Decreases in arterial pressure or bilateral blockade of RVLM GABAA receptors also revealed differential activation, with the latter having a 3- to 4-fold greater effect on sympathetic activity. Our data provide evidence that activation of the rat RVLM increases renal, lumbar, and preganglionic adrenal sympathetic nerve activities concurrently, differentially, and, in some cases, selectively.

scholarly journals ATP-sensitive K+ channel inhibition in rats decreases kidney and skeletal muscle blood flow without increasing sympathetic nerve discharge

2020 ◽  
Vol 278 ◽  
pp. 103444
Author(s):  
Trenton D. Colburn ◽  
Clark T. Holdsworth ◽  
Jesse C. Craig ◽  
Daniel M. Hirai ◽  
Shawnee Montgomery ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Sympathetic Nerve ◽  
Muscle Blood Flow ◽  
K Channel ◽  
Skeletal Muscle Blood Flow ◽  
Channel Inhibition ◽  
Nerve Discharge

Forced oscillations in sympathetic nerve discharge

1992 ◽  
Vol 263 (3) ◽  
pp. R564-R571 ◽  
Author(s):  
Z. S. Huang ◽  
G. L. Gebber ◽  
S. Zhong ◽  
S. M. Barman
Keyword(s):  
Sympathetic Nerve ◽  
Stimulus Frequency ◽  
Wide Band ◽  
Forced Oscillations ◽  
Physiological Noise ◽  
Coupled Nonlinear Oscillators ◽  
Oscillatory State ◽  
Postganglionic Nerve ◽  
Stimulation Of ◽  
Nerve Discharge

Periodic electrical stimulation of the medullary raphe or lateral tegmental field in baroreceptor-denervated cats was used to force the central systems responsible for the 10-Hz and 2- to 6-Hz rhythms in post-ganglionic sympathetic nerve discharge (SND). The 10-Hz rhythm in SND could be entrained either to the frequency of medullary stimulation or to harmonics of the stimulus frequency. The harmonic of the stimulus frequency to which the 10-Hz rhythm was entrained in one postganglionic nerve could be different from that in another nerve. On this basis, we propose that the circuits responsible for the 10-Hz rhythms in SND may be modeled as a system of coupled nonlinear oscillators, each of which either influences one postganglionic nerve or nonuniformly affects different postganglionic nerves. The relatively wide band 2- to 6-Hz component in SND could be forced into a stable oscillatory state by medullary stimulation at frequencies between 3 and 5 Hz. This observation is consistent with the view that the 2- to 6-Hz component reflects the complex behavior of a nonlinear oscillator rather than the output of a physiological noise generator.

Differential control of sympathetic outflow

2001 ◽  
Vol 281 (3) ◽  
pp. R683-R698 ◽  
Author(s):  
Shaun F. Morrison
Keyword(s):  
Aggressive Response ◽  
Sympathetic Outflow ◽  
Autonomic Activity ◽  
Premotor Neurons ◽  
Life Threatening ◽  
Sympathetic Nervous ◽  
The Many ◽  
Differential Control ◽  
Physiological Substrates ◽  
Stimulation Of

With advances in experimental techniques, the early views of the sympathetic nervous system as a monolithic effector activated globally in situations requiring a rapid and aggressive response to life-threatening danger have been eclipsed by an organizational model featuring an extensive array of functionally specific output channels that can be simultaneously activated or inhibited in combinations that result in the patterns of autonomic activity supporting behavior and mediating homeostatic reflexes. With this perspective, the defense response is but one of the many activational states of the central autonomic network. This review summarizes evidence for the existence of tissue-specific sympathetic output pathways, which are likely to include distinct populations of premotor neurons whose target specificity could be assessed using the functional fingerprints developed from characterizations of postganglionic efferents to known targets. The differential responses in sympathetic outflows to stimulation of reflex inputs suggest that the circuits regulating the activity of sympathetic premotor neurons must have parallel access to groups of premotor neurons controlling different functions but that these connections vary in their ability to influence different sympathetic outputs. Understanding the structural and physiological substrates antecedent to premotor neurons that mediate the differential control of sympathetic outflows, including those to noncardiovascular targets, represents a challenge to our current technical and analytic approaches.

Medullary sympathoexcitatory neurons are inhibited by activation of the medial prefrontal cortex in the rat

1996 ◽  
Vol 270 (4) ◽  
pp. R713-R719 ◽  
Author(s):  
A. J. Verberne
Keyword(s):  
Blood Pressure ◽  
Electrical Stimulation ◽  
Prefrontal Cortex ◽  
Arterial Blood Pressure ◽  
Medial Prefrontal Cortex ◽  
Sympathetic Nerve ◽  
Ventrolateral Medulla ◽  
Arterial Blood ◽  
Stimulation Of ◽  
Nerve Discharge

Electrical stimulation of the medial prefrontal cortex (MPFC) reduces arterial blood pressure. To investigate the mechanism of this response, the effects of electrical and chemical stimulation of the MPFC on splanchnic and lumbar sympathetic nerve discharge and on the discharges of barosensitive neurons of the rostral ventrolateral medulla (RVLM) were studied in halothane-anesthetized rats. Electrical stimulation (20 Hz, 1 ms, 100 and sympathoinhibitory responses (reduced discharge of the splanchnic sympathetic nerve). Microinjection of glutamate (10 nmol/100 nl) into the MPFC also reduced arterial blood pressure and sympathetic discharge. Electrical stimulation (0.5 Hz, 1-ms pulse pairs, 3-ms interval, 150-300 microA) produced distinct patterns of splanchnic and lumbar sympathetic nerve discharge. A clear sympathoinhibitory phase with an onset latency of 146 +/- 14 ms was observed only in the case of the splanchnic sympathetic nerve activity. Electrical stimulation at depressor sites within the MPFC also inhibited the discharge of 10 of 21 RVLM barosensitive neurons tested. RVLM neurons were never excited by MPFC stimulation. These results indicate that the MPFC contains neurons that form part of a central sympathoinhibitory pathway.

Activation of slowly conducting medullary raphé-spinal neurons, including serotonergic neurons, increases cutaneous sympathetic vasomotor discharge in rabbit

2005 ◽  
Vol 288 (4) ◽  
pp. R909-R918 ◽  
Author(s):  
Youichirou Ootsuka ◽  
William W. Blessing
Keyword(s):  
Spinal Cord ◽  
Electrical Stimulation ◽  
Conduction Velocity ◽  
Sympathetic Nerve ◽  
Substantial Contribution ◽  
Spinal Neurons ◽  
Thoracic Spinal Cord ◽  
Medullary Raphe ◽  
Stimulation Of ◽  
Nerve Discharge

Neurons in the rostral medullary raphé/parapyramidal region regulate cutaneous sympathetic nerve discharge. Using focal electrical stimulation at different dorsoventral raphé/parapyramidal sites in anesthetized rabbits, we have now demonstrated that increases in ear pinna cutaneous sympathetic nerve discharge can be elicited only from sites within 1 mm of the ventral surface of the medulla. By comparing the latency to sympathetic discharge following stimulation at the ventral raphé site with the corresponding latency following stimulation of the spinal cord [third thoracic (T3) dorsolateral funiculus] we determined that the axonal conduction velocity of raphé-spinal neurons exciting ear pinna sympathetic vasomotor nerves is 0.8 ± 0.1 m/s ( n = 6, range 0.6–1.1 m/s). Applications of the 5-hydroxytryptamine (HT)2A antagonist trans-4-((3 Z)3-[(2-dimethylaminoethyl)oxyimino]-3-(2-fluorophenyl)propen-1-yl)-phenol, hemifumarate (SR-46349B, 80 μg/kg in 0.8 ml) to the cerebrospinal fluid above thoracic spinal cord (T1-T7), but not the lumbar spinal cord (L2-L4), reduced raphé-evoked increases in ear pinna sympathetic vasomotor discharge from 43 ± 9 to 16 ± 6% ( P < 0.01, n = 8). Subsequent application of the excitatory amino acid (EAA) antagonist kynurenic acid (25 μmol in 0.5 ml) substantially reduced the remaining evoked discharge (22 ± 8 to 6 ± 6%, P < 0.05, n = 5). Our conduction velocity data demonstrate that only slowly conducting raphé-spinal axons, in the unmyelinated range, contribute to sympathetic cutaneous vasomotor discharge evoked by electrical stimulation of the medullary raphé/parapyramidal region. Our pharmacological data provide evidence that raphé-spinal neurons using 5-HT as a neurotransmitter contribute to excitation of sympathetic preganglionic neurons regulating cutaneous vasomotor discharge. Raphé-spinal neurons using an EAA, perhaps glutamate, make a substantial contribution to the ear sympathetic nerve discharge evoked by raphé stimulation.

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