scholarly journals Bacillus anthracis lethal toxin alters regulation of visceral sympathetic nerve discharge

2012 ◽  
Vol 112 (6) ◽  
pp. 1033-1040 ◽  
Author(s):  
A. A. Garcia ◽  
R. J. Fels ◽  
L. J. Mosher ◽  
M. J. Kenney
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Bacillus Anthracis ◽  
Sympathetic Nerve ◽  
Critical Role ◽  
Lethal Factor ◽  
Lethal Toxin ◽  
Arterial Blood ◽  
Sympathetic Nervous ◽  
Nerve Discharge

Bacillus anthracis infection is a pathophysiological condition that is complicated by progressive decreases in mean arterial pressure (MAP). Lethal toxin (LeTx) is central to the pathogenesis of B. anthracis infection, and the sympathetic nervous system plays a critical role in physiological regulation of acute stressors. However, the effect of LeTx on sympathetic nerve discharge (SND), a critical link between central sympathetic neural circuits and MAP regulation, remains unknown. We determined visceral (renal, splenic, and adrenal) SND responses to continuous infusion of LeTx [lethal factor (100 μg/kg) + protective antigen (200 μg/kg) infused at 0.5 ml/h for ≤6 h] and vehicle (infused at 0.5 ml/h) in anesthetized, baroreceptor-intact and baroreceptor (sinoaortic)-denervated (SAD) Sprague-Dawley rats. LeTx infusions produced an initial state of cardiovascular and sympathetic nervous system activation in intact and SAD rats. Subsequent to peak LeTx-induced increases in arterial blood pressure, intact rats demonstrated a marked hypotension that was accompanied by significant reductions in SND (renal and splenic) and heart rate (HR) from peak levels. After peak LeTx-induced pressor and sympathoexcitatory responses in SAD rats, MAP, SND (renal, splenic, and adrenal), and HR were progressively and significantly reduced, supporting the hypothesis that LeTx alters the central regulation of sympathetic nerve outflow. These findings demonstrate that the regulation of visceral SND is altered in a complex manner during continuous anthrax LeTx infusions and suggest that sympathetic nervous system dysregulation may contribute to the marked hypotension accompanying B. anthracis infection.

Hypertension and insulin resistance: role of sympathetic nervous system activity

1992 ◽  
Vol 263 (5) ◽  
pp. E935-E942 ◽  
Author(s):  
M. A. Supiano ◽  
R. V. Hogikyan ◽  
L. A. Morrow ◽  
F. J. Ortiz-Alonso ◽  
W. H. Herman ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Multiple Regression Model ◽  
Metabolic Effects ◽  
Plasma Norepinephrine ◽  
Intravenous Glucose ◽  
Arterial Blood ◽  
Sympathetic Nervous ◽  
Intravenous Glucose Tolerance Tests

he purpose of this study was to test the hypothesis that heightened sympathetic nervous system (SNS) activity contributes to the mechanism by which hypertension is associated with insulin resistance in humans. We performed frequently sampled intravenous glucose tolerance tests to determine tissue sensitivity to metabolic effects of insulin (SI) and measured plasma norepinephrine (NE) levels in 21 normotensive and 14 hypertensive Caucasian subjects. Compared with the normotensive subjects, hypertensive subjects had decreased SI (5.4 +/- 0.5 vs. 4.0 +/- 0.7 x 10(-5) x min-1 x pM-1; P = 0.03) but similar plasma NE levels (normotensive: 1.82 +/- 0.12 vs. hypertensive: 1.73 +/- 0.16 nM; P = 0.23). In a multiple regression model, only body mass index (BMI) and mean arterial blood pressure (MABP) were significant independent predictors of SI [SI = (-0.513)(BMI) + (-0.058)(MABP) + 23.6; r = 0.748; P = 0.0001]; age, plasma glucose, epinephrine, and NE level did not enter this model. As an additional test of this hypothesis, seven hypertensive subjects were restudied after 10 days of guanadrel therapy to determine whether SI would increase during suppression of SNS activity by guanadrel. Despite a significant reduction in plasma NE levels with guanadrel (baseline: 1.63 +/- 0.18 vs. guanadrel: 0.99 +/- 0.14 nM; P = 0.01), there was no significant change in SI (baseline: 2.97 +/- 0.78 vs. guanadrel: 2.41 +/- 0.54 x 10(-5).min-1 x pM-1; analysis of variance P = 0.57). We conclude that, in the Caucasian population we studied, heightened SNS activity is not essential for the insulin resistance observed in hypertensive humans.

Dissociation of sympathetic nervous system and adrenal medullary responses

1984 ◽  
Vol 247 (1) ◽  
pp. E35-E40 ◽  
Author(s):  
J. B. Young ◽  
R. M. Rosa ◽  
L. Landsberg
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Adrenal Medulla ◽  
Sympathetic Nerve ◽  
Relative Importance ◽  
Peripheral Tissues ◽  
Experimental Animals ◽  
Sympathetic Nervous

The relative importance of sympathetic nerve (SNS) activity and adrenal medullary secretion in various physiological situations has generally been inferred from measurements of norepinephrine (NE) and epinephrine (E), respectively, in urine or plasma. Increasing evidence, however, indicates that under certain conditions the adrenal medulla may release substantial amounts of NE as well as E. In several of these circumstances, estimates of SNS activity based on the measurement of NE turnover in peripheral tissues of experimental animals indicate diminished SNS function, a reduction that is independent of adrenal medullary secretion. These reciprocal alterations in SNS and adrenal medullary activity fall into two patterns. First, when SNS activity is suppressed by fasting, adrenal medullary responses to various stimuli are enhanced. Second, for certain stimuli the SNS response is biphasic, with an initial suppression followed by subsequent stimulation; during the first phase adrenal medullary secretion is markedly increased. The physiological contribution of the adrenal medulla, therefore, would be particularly important under conditions of SNS suppression.

CNS origins of the sympathetic nervous system outflow to brown adipose tissue

1999 ◽  
Vol 276 (6) ◽  
pp. R1569-R1578 ◽  
Author(s):  
Maryam Bamshad ◽  
C. Kay Song ◽  
Timothy J. Bartness
Keyword(s):  
Nervous System ◽  
Adipose Tissue ◽  
Sympathetic Nervous System ◽  
Brown Adipose Tissue ◽  
Pseudorabies Virus ◽  
Critical Role ◽  
Hypothalamic Nucleus ◽  
Brown Adipose ◽  
Sympathetic Nervous ◽  
Diet Induced Thermogenesis

Brown adipose tissue (BAT) plays a critical role in cold- and diet-induced thermogenesis. Although BAT is densely innervated by the sympathetic nervous system (SNS), little is known about the central nervous system (CNS) origins of this innervation. The purpose of the present experiment was to determine the neuroanatomic chain of functionally connected neurons from the CNS to BAT. A transneuronal viral tract tracer, Bartha’s K strain of the pseudorabies virus (PRV), was injected into the interscapular BAT of Siberian hamsters. The animals were killed 4 and 6 days postinjection, and the infected neurons were visualized by immunocytochemistry. PRV-infected neurons were found in the spinal cord, brain stem, midbrain, and forebrain. The intensity of labeled neurons in the forebrain varied from heavy infections in the medial preoptic area and paraventricular hypothalamic nucleus to few infections in the ventromedial hypothalamic nucleus, with moderate infections in the suprachiasmatic and lateral hypothalamic nuclei. These results define the SNS outflow from the brain to BAT for the first time in any species.

Interactions between ANG II, sympathetic nervous system, and baroreceptor reflexes in regulation of blood pressure

1992 ◽  
Vol 262 (6) ◽  
pp. E763-E778 ◽  
Author(s):  
I. A. Reid
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Blood Pressure Control ◽  
Cardiovascular Responses ◽  
Pressure Control ◽  
Ang Ii ◽  
Arterial Blood ◽  
Baroreceptor Reflexes ◽  
Sympathetic Nervous

The renin-angiotensin system plays an important role in the regulation of arterial blood pressure and in the development of some forms of clinical and experimental hypertension. It is an important blood pressure control system in its own right but also interacts extensively with other blood pressure control systems, including the sympathetic nervous system and the baroreceptor reflexes. Angiotensin (ANG) II exerts several actions on the sympathetic nervous system. These include a central action to increase sympathetic outflow, stimulatory effects on sympathetic ganglia and the adrenal medulla, and actions at sympathetic nerve endings that serve to facilitate sympathetic neurotransmission. ANG II also interacts with baroreceptor reflexes. For example, it acts centrally to modulate the baroreflex control of heart rate, and this accounts for its ability to increase blood pressure without causing a reflex bradycardia. The physiological significance of these actions of ANG II is not fully understood. Most evidence indicates that the actions of ANG to enhance sympathetic activity do not contribute significantly to the pressor response to exogenous ANG II. On the other hand, there is considerable evidence that the actions of endogenous ANG II on the sympathetic nervous system enhance the cardiovascular responses elicited by activation of the sympathetic nervous system.

The sympathetic muscle metaboreflex is not different in the third trimester in normotensive pregnant women.

2020 ◽  
Author(s):  
Rachel J. Skow ◽  
Andrew R. Steele ◽  
Graham M. Fraser ◽  
Margie H. Davenport ◽  
Craig D. Steinback
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Pregnant Women ◽  
Isometric Handgrip ◽  
Third Trimester ◽  
Muscle Metaboreflex ◽  
The Third ◽  
Arterial Blood ◽  
Sympathetic Nervous

Isometric handgrip (IHG) is used to assess sympathetic nervous system responses to exercise and may be useful at predicting hypertension in both pregnant and non-pregnant populations. We have previously observed altered sympathetic nervous system control of blood pressure in late pregnancy. Therefore, we measured muscle sympathetic nerve activity (MSNA) and blood pressure during muscle metaboreflex activation (IHG) in normotensive pregnant women in the third trimester compared to healthy non-pregnant women. Nineteen pregnant (32±3wks gestation) and fourteen non-pregnant women were matched for age, non/pre-pregnant BMI, and parity. MSNA (microneurography), heart rate (ECG), and arterial blood pressure (Finometer) were continuously recorded during ten minutes of rest, and then during two-minutes of IHG at 30% of maximal voluntary contraction, and two-minutes of post-exercise circulatory occlusion (PECO). Baseline SNA was elevated in pregnant (41±11 bursts/min) compared to non-pregnant women (27 ± 9 bursts/minute; p=0.005); however, the sympathetic baroreflex gain and neurovascular transduction were not different between groups (p=0.62 and p=0.32, respectively). During IHG and PECO there was no significant differences in the pressor response (∆MAP) during IHG and PECO was not different between groups (p=0.25, main effect of group) nor the sympathetic response (interaction effect: p=0.16, 0.25, and 0.27 for burst frequency, burst incidence, and total SNA respectively). These data suggest that pregnant women who have maintained sympathetic baroreflex and neurovascular transduction also have similar sympathetic and pressor responses during exercise.

scholarly journals The adipokine chemerin amplifies electrical field-stimulated contraction in the isolated rat superior mesenteric artery

2016 ◽  
Vol 311 (2) ◽  
pp. H498-H507 ◽  
Author(s):  
Emma S. Darios ◽  
Brittany M. Winner ◽  
Trevor Charvat ◽  
Antoni Krasinksi ◽  
Sreenivas Punna ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Superior Mesenteric Artery ◽  
Sympathetic Nerve ◽  
Mesenteric Artery ◽  
Sympathetic Innervation ◽  
Electrical Field ◽  
Perivascular Adipose Tissue ◽  
Sympathetic Nervous

The adipokine chemerin causes arterial contraction and is implicated in blood pressure regulation, especially in obese subjects with elevated levels of circulating chemerin. Because chemerin is expressed in the perivascular adipose tissue (PVAT) that surrounds the sympathetic innervation of the blood vessel, we tested the hypothesis that chemerin (endogenous and exogenous) amplifies the sympathetic nervous system in mediating electrical field-stimulated (EFS) contraction. The superior mesenteric artery, with or without PVAT and with endothelium and sympathetic nerve intact, was mounted into isolated tissue baths and used for isometric contraction and stimulation. Immunohistochemistry validated a robust expression of chemerin in the PVAT surrounding the superior mesenteric artery. EFS (0.3–20 Hz) caused a frequency-dependent contraction in isolated arteries that was reduced by the chemerin receptor ChemR23 antagonist CCX832 alone (100 nM; with, but not without, PVAT), but not by the inactive congener CCX826 (100 nM). Exogenous chemerin-9 (1 μM)-amplified EFS-induced contraction in arteries (with and without PVAT) was blocked by CCX832 and the α-adrenergic receptor antagonist prazosin. CCX832 did not directly inhibit, nor did chemerin directly amplify, norepinephrine-induced contraction. Whole mount immunohistochemical experiments support colocalization of ChemR23 with the sympathetic nerve marker tyrosine hydroxylase in superior mesenteric PVAT and, to a lesser extent, in arteries and veins. These studies support the idea that exogenous chemerin modifies sympathetic nerve-mediated contraction through ChemR23 and that ChemR23 may be endogenously activated. This is significant because of the well-appreciated role of the sympathetic nervous system in blood pressure control.

Frequency response characteristic of sympathetic-mediated vasomotor waves in conscious rats

1996 ◽  
Vol 271 (4) ◽  
pp. H1416-H1422 ◽  
Author(s):  
H. M. Stauss ◽  
K. C. Kregel
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Frequency Response ◽  
Arterial Blood Pressure ◽  
Nerve Stimulation ◽  
Splanchnic Nerve ◽  
Conscious Rats ◽  
Arterial Blood ◽  
Sympathetic Nervous

Power spectrum analysis of arterial blood pressure (BP) and heart rate (HR) has been used to investigate autonomic nervous system activity. Sympathetic-mediated vasomotor tone has been attributed to the BP power at frequencies between 0.05 and 0.15 Hz in humans and dogs and between 0.2 and 0.8 Hz in rats. In contrast, it has been suggested that the sympathetic nervous system is too sluggish to transmit frequencies higher than 0.017 Hz in dogs. Thus we investigated the frequency-response characteristics of the transmission of peripheral sympathetic nerve discharge to peripheral vascular resistance and arterial blood pressure in conscious rats. Eleven rats were instrumented with arterial catheters, nerve electrodes on the sympathetic splanchnic nerve, and flow probes on the superior mesenteric artery. The splanchnic nerve was cut proximal to the electrode to avoid afferent nerve stimulation. The next day the nerve was stimulated at frequencies of 0.05, 0.1, 0.2, 0.5, 1.0, and 2.0 Hz while mesenteric blood flow, BP, and HR were recorded in conscious rats. Mesenteric resistance (MR) was calculated off-line. Nerve stimulation at 0.05, 0.1, 0.2, 0.5, and 1.0 Hz significantly increased the power in MR at these respective frequencies. The greatest response was found between 0.2 and 0.5 Hz. These oscillations in MR were translated to oscillations in BP, but not in HR. Nerve stimulation on the second day, when the nerve was degenerated, did not elicit oscillations in MR or BP. We conclude that the peripheral sympathetic nervous system in rats can transmit signals at frequencies higher than those traditionally assigned to sympathetic vasomotor activity in several species, including humans, and may even overlap with the respiration-related high-frequency range.

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 Sympathetic Blocks Provided Sustained Pain Relief in a Patient with Refractory Painful Diabetic Neuropathy

2012 ◽  
Vol 2012 ◽  
pp. 1-5 ◽  
Author(s):  
Jianguo Cheng ◽  
Anuj Daftari ◽  
Lan Zhou
Keyword(s):  
Nervous System ◽  
Pain Relief ◽  
Sympathetic Nervous System ◽  
Diabetic Neuropathy ◽  
Critical Role ◽  
Sensory Neuropathy ◽  
Painful Diabetic Neuropathy ◽  
Nerve Blocks ◽  
Sympathetic Nervous ◽  
Sympathetic Blocks

The sympathetic nervous system has been implicated in pain associated with painful diabetic neuropathy. However, therapeutic intervention targeted at the sympathetic nervous system has not been established. We thus tested the hypothesis that sympathetic nerve blocks significantly reduce pain in a patient with painful diabetic neuropathy who has failed multiple pharmacological treatments. The diagnosis of small fiber sensory neuropathy was based on clinical presentations and confirmed by skin biopsies. A series of 9 lumbar sympathetic blocks over a 26-month period provided sustained pain relief in his legs. Additional thoracic paravertebral blocks further provided control of the pain in the trunk which can occasionally be seen in severe diabetic neuropathy cases, consequent to extensive involvement of the intercostal nerves. These blocks provided sustained and significant pain relief and improvement of quality of life over a period of more than two years. We thus provided the first clinical evidence supporting the notion that sympathetic nervous system plays a critical role in painful diabetic neuropathy and sympathetic blocks can be an effective management modality of painful diabetic neuropathy. We concluded that the sympathetic nervous system is a valuable therapeutic target of pharmacological and interventional modalities of treatments in painful diabetic neuropathy patients.

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