Microneurography: how the technique developed and its role in the investigation of the sympathetic nervous system

2004 ◽  
Vol 96 (4) ◽  
pp. 1262-1269 ◽  
Author(s):  
Åke B. Vallbo ◽  
Karl-Erik Hagbarth ◽  
B. Gunnar Wallin
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Historical Review ◽  
Nerve Activity ◽  
Sympathetic Nervous

A historical review is given of the development of microneurography and its application for studies of sympathetic nerve activity in humans.

Arterial pressure lability and renal sympathetic nerve activity are dissociated in SAD rats

1992 ◽  
Vol 263 (3) ◽  
pp. R639-R646 ◽  
Author(s):  
C. Barres ◽  
S. J. Lewis ◽  
H. J. Jacob ◽  
M. J. Brody
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
High Variability ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Sympathetic Nervous ◽  
Renal Sympathetic

The purpose of this study was to determine whether the sympathetic nervous system drives the high variability of arterial pressure (AP) observed after sinoaortic denervation (SAD) in rats. One or fourteen days after SAD, rats were instrumented chronically to record mean AP (MAP), heart rate (HR), and renal sympathetic nerve activity (RSNA) in the conscious unrestrained state. Acute SAD increased MAP, HR, RSNA, and variability of MAP and decreased variability of both HR and RSNA. In rats with chronic SAD, variability of MAP remained high, whereas MAP, HR, RSNA, and variability of HR and RSNA returned to normal levels. Correlation analysis showed that, in sham-operated rats, AP and RSNA were negatively correlated in 90% of cases. In contrast, rats with both acute and chronic SAD exhibited only 30% negative and 25% positive correlations. These results indicate that 1) low AP variability in intact rats results from baroreflex-mediated inversely related fluctuations in RSNA and HR and 2) high variability of AP after acute and chronic SAD is correlated infrequently with RSNA. Because lability is reduced by interventions that block the sympathetic nervous system, we conclude that lability of AP associated with SAD appears to be mediated largely by a permissive role of sympathetic activity.

scholarly journals Recording sympathetic nerve activity chronically in rats: surgery techniques, assessment of nerve activity, and quantification

2013 ◽  
Vol 305 (10) ◽  
pp. H1407-H1416 ◽  
Author(s):  
Sean D. Stocker ◽  
Martin S. Muntzel
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Sympathetic Nerve ◽  
Time Course ◽  
Sympathetic Nerve Activity ◽  
Surgical Approaches ◽  
Nerve Activity ◽  
Disease States ◽  
Nervous System Function ◽  
Sympathetic Nervous

The sympathetic nervous system plays a pivotal role in homeostasis through its direct innervation and functional impact on a variety of end organs. In rats, a number of methods are available to assess sympathetic nervous system function. Traditionally, direct recording of sympathetic nerve activity (SNA) has been restricted to acute, anesthetized preparations or conscious animals within a few days after electrode implantation. However, these approaches provide short-term data in studies designed to investigate changes in SNA during chronic disease states. Over the last several years, chronic SNA recording has been pioneered in rabbits and more recently in rats. The purpose of this article is to provide insights and a “how to” guide for chronic SNA recordings in rats based on experiences from two independent laboratories. We will present common methodologies used to chronically record SNA, characteristics and methods to distinguish sympathetic bursts versus electrical artifacts (and provide corresponding audio clips when available), and provide suggestions for analysis and presentation of data. In many instances, these same guidelines are applicable to acute SNA recordings. Using the surgical approaches described herein, both laboratories have been able to chronically record SNA in >50% of rats for a duration >3 wk. The ability to record SNA over the time course of several weeks will, undoubtedly, greatly impact the field of autonomic and cardiovascular physiology.

Differential sympathetic responses initiated by angiotensin and sodium chloride

1983 ◽  
Vol 245 (1) ◽  
pp. R60-R68 ◽  
Author(s):  
J. C. Tobey ◽  
H. K. Fry ◽  
C. S. Mizejewski ◽  
G. D. Fink ◽  
L. C. Weaver
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Sympathetic Outflow ◽  
Ang Ii ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Renal Nerve Activity ◽  
Sympathetic Nervous

Angiotensin II (ANG II) and NaCl act on central receptors to cause pressor responses that may be mediated in part by the sympathetic nervous system. The inhibitory or excitatory nature of effects on central sympathetic outflow are not well defined. This study was undertaken to evaluate further the potential contribution of the sympathetic nervous system to central actions of angiotensin or hypertonic NaCl. Experiments were performed using anesthetized, sinoaortic denervated, vagotomized cats. Intracarotid injection of NaCl produced increased splenic sympathetic nerve activity and decreased renal sympathetic nerve activity. Intracerebroventricular (icv) administration of NaCl caused slight excitatory responses in splenic nerves and no change in renal nerve activity. Intracarotid injection of ANG II caused significantly greater splenic than renal excitation. Administration of ANG II icv caused excitation of splenic nerve activity and no change in renal nerve activity. These findings illustrate that stimulation of sodium-sensitive and angiotensin-sensitive CNS receptors produces differential responses in sympathetic outflow. These differential sympathetic responses may contribute to the complex cardiovascular responses to increased plasma or brain concentrations of angiotensin or sodium.

Attenuated baroreflex control of sympathetic nerve activity after cardiovascular deconditioning in rats

1998 ◽  
Vol 274 (5) ◽  
pp. R1397-R1405 ◽  
Author(s):  
J. A. Moffitt ◽  
C. M. Foley ◽  
J. C. Schadt ◽  
M. H. Laughlin ◽  
E. M. Hasser
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Orthostatic Intolerance ◽  
Hindlimb Unloading ◽  
Nerve Activity ◽  
Baroreflex Control ◽  
Cardiovascular Deconditioning ◽  
Sympathetic Nervous

The effect of cardiovascular deconditioning on baroreflex control of the sympathetic nervous system was evaluated after 14 days of hindlimb unloading (HU) or the control condition. Rats were chronically instrumented with catheters and sympathetic nerve recording electrodes for measurement of mean arterial pressure (MAP) and heart rate (HR) and recording of lumbar (LSNA) or renal (RSNA) sympathetic nerve activity. Experiments were conducted 24 h after surgery, with the animals in a normal posture. Baroreflex function was assessed using a logistic function that related HR and LSNA or RSNA to MAP during infusion of phenylephrine and nitroprusside. Baroreflex influence on HR was not affected by HU. Maximum baroreflex-elicited LSNA was significantly reduced in HU rats (204 ± 11.9 vs. 342 ± 30.6% baseline LSNA), as was maximum reflex gain (−4.0 ± 0.6 vs. −7.8 ± 1.3 %LSNA/mmHg). Maximum baroreflex-elicited RSNA (259 ± 10.8 vs. 453 ± 28.0% baseline RSNA), minimum baroreflex-elicited RSNA (−2 ± 2.8 vs. 13 ± 4.5% baseline RSNA), and maximum gain (−5.8 ± 0.5 vs. −13.6 ± 3.1 %RSNA/mmHg) were significantly decreased in HU rats. Results demonstrate that baroreflex modulation of sympathetic nervous system activity is attenuated after cardiovascular deconditioning in rodents. Data suggest that alterations in the arterial baroreflex may contribute to orthostatic intolerance after a period of bedrest or spaceflight in humans.

Exercise training attenuates increases in lumbar sympathetic nerve activity produced by stimulation of the rostral ventrolateral medulla

2007 ◽  
Vol 102 (2) ◽  
pp. 803-813 ◽  
Author(s):  
Patrick J. Mueller
Keyword(s):  
Nervous System ◽  
Mean Arterial Pressure ◽  
Exercise Training ◽  
Sympathetic Nervous System ◽  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Ventrolateral Medulla ◽  
Nerve Activity ◽  
Sympathetic Nervous

Exercise training (ExTr) has been associated with blunted activation of the sympathetic nervous system in several animal models and in some human studies. Although these data are consistent with the hypothesis that ExTr reduces the incidence of cardiovascular diseases via reduced sympathoexcitation, the mechanisms are unknown. The rostral ventrolateral medulla (RVLM) is important in control of sympathetic nervous system activity in both physiological and pathophysiological states. The purpose of the present study was to test the hypothesis that ExTr results in reduced sympathoexcitation mediated at the level of the RVLM. Male Sprague-Dawley rats were treadmill trained or remained sedentary for 8–10 wk. RVLM microinjections were performed under Inactin anesthesia while mean arterial pressure, heart rate, and lumbar sympathetic nerve activity (LSNA) were recorded. Bilateral microinjections of the GABAA antagonist bicuculline (5 mM, 90 nl) into the RVLM increased LSNA in sedentary animals (169 ± 33%), which was blunted in ExTr animals (100 ± 22%, P < 0.05). Activation of the RVLM with unilateral microinjections of glutamate (10 mM, 30 nl) increased LSNA in sedentary animals (76 ± 13%), which was also attenuated by training (26 ± 2%, P < 0.05). Bilateral microinjections of the ionotropic glutamate receptor antagonist kynurenate (40 mM, 90 nl) produced small increases in mean arterial pressure and LSNA that were similar between groups. Results suggest that ExTr may reduce increases in LSNA due to reduced activation of the RVLM. Conversely, we speculate that the relatively enhanced activation of LSNA in sedentary animals may be related to the increased incidence of cardiovascular disease associated with a sedentary lifestyle.

Cardiac-related rhythms in sympathetic nerve activity in preterm fetal sheep

2007 ◽  
Vol 293 (1) ◽  
pp. R185-R190 ◽  
Author(s):  
Lindsea C. Booth ◽  
Laura Bennet ◽  
Carolyn J. Barrett ◽  
Sarah-Jane Guild ◽  
Guido Wassink ◽  
...  
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Cardiac Cycle ◽  
Diastolic Pressure ◽  
Nerve Activity ◽  
Average Delay ◽  
Fetal Sheep ◽  
Sympathetic Nervous

Extensive studies in the adult have demonstrated that the sympathetic nervous system plays a central role in cardiovascular control. The maturation of the sympathetic nervous system before birth is poorly understood. In the present study, we directly recorded renal sympathetic nerve activity (renal SNA) in five preterm fetal sheep (99 ± 1 days gestation; term is 147 days). Recordings were performed in utero using a telemetry-based technique to alleviate movement artifact without anesthesia or paralysis. The preterm fetuses exhibited a coordinated discharge pattern in renal SNA, indicating many individual neurons active at approximately the same time. This is consistent with that observed previously in adult animals, although the frequency of the bursts was relatively low (0.5 ± 0.1 Hz). The discharges in renal SNA were entrained to the cardiac cycle (average delay between diastolic pressure and maximum renal SNA 319 ± 1 ms). The entrainment of the sympathetic discharges to the cardiac cycle indicates phasic baroreceptor input and that the underlying circuits controlling SNA within the central nervous system are active in premature fetuses.

Sympathetic nerve activity during prolonged rhythmic forearm exercise

1994 ◽  
Vol 76 (3) ◽  
pp. 1077-1081 ◽  
Author(s):  
B. A. Batman ◽  
J. C. Hardy ◽  
U. A. Leuenberger ◽  
M. B. Smith ◽  
Q. X. Yang ◽  
...  
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Sympathetic Nerve ◽  
Maximal Voluntary Contraction ◽  
Sympathetic Nerve Activity ◽  
Voluntary Contraction ◽  
Nerve Activity ◽  
Sympathetic Nervous ◽  
Rhythmic Exercise ◽  
Forearm Exercise

Exercise is a potent stimulus to activate the sympathetic nervous system. Previous work suggests that metabolite-sensitive muscle afferents are activated near the point of fatigue, and, when activated, they determine the muscle sympathetic nerve activity (MSNA) response to isometric forearm exercise. Yet, studies using a more prolonged rhythmic exercise paradigm suggest that the sympathetic nervous system can be activated in a more graded fashion. The purpose of this study was to determine whether metaboreceptor stimulation would also be responsible for MSNA responses to prolonged rhythmic isotonic forearm exercise. Subjects (n = 16) performed rhythmic isotonic forearm exercise at 25% maximal voluntary contraction for 30 min as we measured MSNA (microneurography). We observed progressive increases in MSNA with a peak increase of 161 units from a baseline value of 180 units. We also performed posthandgrip circulatory arrest (PHG-CA) in nine of these subjects. This maneuver isolates the metaboreceptor contribution to MSNA. During PHG-CA, delta MSNA values were not different from those observed during a freely perfused recovery period (n = 7). We also compared MSNA responses during the rhythmic paradigm with those seen during a static protocol at 40% of maximal voluntary contraction in five subjects. The two types of exercise caused similar increases in MSNA, but only the static paradigm was associated with a sustained MSNA response during PHG-CA. Finally, 31P-nuclear magnetic resonance was used to evaluate muscle metabolic responses during rhythmic and static forearm exercise (n = 6). Static exercise caused muscle acidosis and an increase in H2PO4-, whereas rhythmic exercise had no effect on muscle metabolism.(ABSTRACT TRUNCATED AT 250 WORDS)

Forearm training attenuates sympathetic responses to prolonged rhythmic forearm exercise

1996 ◽  
Vol 81 (4) ◽  
pp. 1778-1784 ◽  
Author(s):  
Lawrence Sinoway ◽  
Jeffrey Shenberger ◽  
Gretchen Leaman ◽  
Robert Zelis ◽  
Kristen Gray ◽  
...  
Keyword(s):  
Heart Rate ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Voluntary Contraction ◽  
Nerve Activity ◽  
Sympathetic Nervous ◽  
Sympathetic Responses ◽  
Forearm Exercise

Sinoway, Lawrence, Jeffrey Shenberger, Gretchen Leaman, Robert Zelis, Kristen Gray, Robert Baily, and Urs Leuenberger.Forearm training attenuates sympathetic responses to prolonged rhythmic forearm exercise. J. Appl. Physiol. 81(4): 1778–1784, 1996.—We previously demonstrated that nonfatiguing rhythmic forearm exercise at 25% maximal voluntary contraction (12 2-s contractions/min) evokes sympathoexcitation without significant engagement of metabolite-sensitive muscle afferents (B. A. Batman, J. C. Hardy, U. A. Leuenberger, M. B. Smith, Q. X. Yang, and L. I. Sinoway. J. Appl. Physiol. 76: 1077–1081, 1994). This is in contrast to the sympathetic nervous system responses observed during fatiguing static forearm exercise where metabolite-sensitive afferents are the key determinants of sympathetic activation. In this report we examined whether forearm exercise training would attenuate sympathetic nervous system responses to rhythmic forearm exercise. We measured heart rate, mean arterial blood pressure (MAP), muscle sympathetic nerve activity (microneurography), plasma norepinephrine (NE), and NE spillover and clearance (tritiated NE kinetics) during nonfatiguing rhythmic forearm exercise before and after a 4-wk unilateral forearm training paradigm. Training had no effect on forearm mass, maximal voluntary contraction, or heart rate but did attenuate the increase in MAP (increase in MAP: from 15.2 ± 1.8 before training to 11.4 ± 1.4 mmHg after training; P < 0.017), muscle sympathetic nerve activity (increase in bursts: from 10.8 ± 1.4 before training to 6.2 ± 1.1 bursts/min after training; P < 0.030), and the NE spillover (increase in arterial spillover: from 1.3 ± 0.2 before training to 0.6 ± 0.2 nmol ⋅ min−1 ⋅ m−2after training, P < 0.014; increase in venous spillover: from 2.0 ± 0.6 before training to 1.0 ± 0.5 nmol ⋅ min−1 ⋅ m−2after training, P < 0.037) seen in response to exercise performed by the trained forearm. Thus forearm training reduces sympathetic responses during a nonfatiguing rhythmic handgrip paradigm that does not engage muscle metaboreceptors. We speculate that this effect is due to a conditioning-induced reduction in mechanically sensitive muscle afferent discharge.

Suppression of sympathetic nervous system is involved in hypotension and bradycardia during hemofiltration in anesthetized dogs

1995 ◽  
Vol 73 (10) ◽  
pp. 1495-1501 ◽  
Author(s):  
Tetsuya Hayashi ◽  
Toshishige Shibamoto ◽  
Yoshihiro Yamaguchi ◽  
Hong-Gang Wang ◽  
Satoshi Tanaka
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Venous Pressure ◽  
Central Venous ◽  
Induced Hypotension ◽  
Anesthetized Dogs ◽  
Sympathetic Nervous

Hypotension occurring during hemodialysis is often accompanied by paradoxical bradycardia. However, the mechanism is poorly understood. This study was designed to determine the role of the sympathetic nervous system in hemodialysis-induced hypotension and bradycardia. We measured efferent sympathetic nerve activities to the heart (CNA), kidney (RNA), liver (HNA), spleen (SpNA), and adrenal gland (AdNA), along with heart rate (HR), blood pressure (BP), central venous pressure (CVP), and left atrial pressure (LAP) during hemofiltration performed at a rate of 0.3 mL∙kg−1∙min−1 for 30 min in anesthetized dogs. The response to hemorrhage was also studied at the same bleeding speed. Hemorrhage caused a decrease in BP (−18 ± 1 mmHg; 1 mmHg = 133.3 Pa) with reflex increases in HR (7 ± 2 beats/min) and sympathetic nerve activities. In contrast, hemofiltration caused a decrease in CNA (85 ± 18%), HNA (86 ± 11%), and SpNA (88 ± 11%) with greater decreases in BP (−43 ± 10 mmHg) and HR (−27 ± 14 beats/min) than hemorrhage. During hemofiltration, the decreases in BP, HR, CNA, HNA, and SpNA were attenuated after vagotomy. Hematocrit increased by 6.5% at 30 min after hemofiltration, whereas it decreased by 4.3% after hemorrhage. These results suggest that hemofiltration suppresses the sympathetic nervous system, resulting in decreases in HR and BP. Furthermore, this sympathetic suppression during hemofiltration is mediated by vagal afferents.Key words: hemodialysis, baroreceptor reflex, sympathetic nerve activity, hemorrhage, vagus nerve.

P4388Acute detrimental effects of e-cigarette and tobacco cigarette smoking on blood pressure and sympathetic nerve activity in healthy subjects

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
K Dimitriadis ◽  
C Tsioufis ◽  
K Kontantinou ◽  
I Liatakis ◽  
E Andrikou ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Nervous System ◽  
Cigarette Smoking ◽  
Sympathetic Nerve ◽  
Healthy Subjects ◽  
Sympathetic Nerve Activity ◽  
Nerve Activity ◽  
Tobacco Cigarette ◽  
Sympathetic Nervous

Abstract Background/Introduction Tobacco cigarette smoking is related with atherosclerosis progression, blood pressure increase and changes in sympathetic nerve activity. However, there are scarce data on the impact of e-cigarettes that have been proposed as less harmful alternatives on the cardiovascular system and sympathetic drive. Purpose This study aimed to assess the acute effects of tobacco cigarettes, e-cigarettes and sham smoking on blood pressure and sympathetic nervous system in healthy subjects. Methods We studied 10 normotensive male habitual smokers (mean age 33 years, body mass index: 24.1 kg/m2, office blood pressure=117/72 mmHg) free of cardiovascular disease. The study design was randomized and placebo controlled with 3 experimental sessions (sham smoking, tobacco cigarette smoking, and e-cigarette smoking) in random order, each session on a separate day. Subjects smoked 2 tobacco cigarettes containing 1.1 mg nicotine or simulate smoking (sham smoking) with the 2 cigarettes separated by 5 minutes, while 45 minutes after finishing the second cigarette, subjects smoked a third cigarette or sham cigarette. Additionally, participants smoked e-cigarettes for a period of 5 and 30 minutes. In all occasions, sympathetic drive was assessed by muscle sympathetic nerve activity (MSNA) (baroreflex-dependent) and skin sympathetic nerve activity (SSNA) (baroreflex-independent) based on established methodology (microneurography). Results After the first, second and third tobacco cigarette smoking there was markedly and significantly increase in mean arterial pressure (by 11.2±1.4%, 12.3±1.3% and 13.1±1.4%, respectively, p<0.05 for all) and heart rate (by 25.1±3.7%, 26.3±2.7% and 25.9±3.7%, respectively, p<0.05 for all). Similarly e-cigarette smoking at 5 and 30 minutes was accompanied by augmentation of mean arterial pressure (by 10.9±1.2% and 12.8±1.4%, respectively, p<0.05 for both) and heart rate (by 22.5±3.3% and 23.9±3.8%, respectively, p<0.05 for both). Regarding the effect on sympathetic nervous system, the first, second and third tobacco cigarette smoking was accompanied by lower MSNA (by 28.1±4.4%, 29.6±5.3% and 30.1±5.2%, respectively, p<0.05 for all), whereas SSNA was increased (by 98.2±19.4%, 100.2±22.7% and 101.5±21.6%, respectively, p<0.05 for all). Additionally, e-cigarette smoking at 5 and 30 minutes caused a decrease in MSNA (by 26.9±3.6%, and 28.3±5.1%, respectively, p<0.05 for both), and an augmentation in SSNA (by 97.9±20.1% and 100.9±20.6%, respectively, p<0.05 for both). Sham smoking was devoid of any effects on blood pressure, MSNA and SSNA. Conclusions E-cigarette smoking acutely increases blood pressure and has a detrimental effect on sympathetic nerve activity regulation similar to tobacco smoking in healthy subjects. Our findings underscore the negative impact of e-cigarettes on cardiovascular and autonomic nervous system and could aid further recommendation in their use.

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