Cervical preganglionic sympathetic nerve activity and chemoreflexes in the cat

1987 ◽  
Vol 62 (4) ◽  
pp. 1713-1720 ◽  
Author(s):  
S. Matsumoto ◽  
A. Mokashi ◽  
S. Lahiri
Keyword(s):  
Nervous System ◽  
Steady State ◽  
Sympathetic Nervous System ◽  
Carotid Body ◽  
Sympathetic Nerve ◽  
Base Line ◽  
Respiratory Drive ◽  
Steady State Levels ◽  
Sympathetic Nervous ◽  
Arterial Po2

The role of chemoreflexes originating from carotid body and central chemoreceptors in the regulation of cervical preganglionic sympathetic nerve (PSN) activity was studied in anesthetized and spontaneously breathing cats. PSN efferents which responded to hypoxia were selected for the study. The PSN activity, breath-by-breath inspiratory tidal volume, tracheal PO2 and PCO2, and arterial systemic blood pressure were recorded simultaneously. The responses of PSN efferents to transient changes in and steady-state levels of arterial PO2 and PCO2 and to graded bolus injections of intravenous sodium cyanide (50–100 micrograms), nicotine (50–100 micrograms), and dopamine hydrochloride (30–60 micrograms) were compared before and after bilateral section of carotid sinus nerves (CSN). CSN section raised the base-line PSN activity and practically eliminated the responses to brief pharmacological stimuli, but it did not eliminate the responses to transient changes in and steady-state levels of arterial PO2 and PCO2. However, CSN section diminished PSN responses and abolished ventilatory responses to hypoxia. Thus the PSN response to hypoxia was partly independent of peripheral chemoreflex and of respiratory drive. We conclude that carotid body chemoreflex elicits fast PSN responses and that a moderate decline in arterial PO2 causes an additional slow, direct excitation of sympathetic nervous system. The latter indicates O2 chemosensitivity of the system in the physiological range of arterial PO2. This O2-sensing property may allow sympathetic nervous system to initiate chemoreflex responses independent of the peripheral chemoreceptors.

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.

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.

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.

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.

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.

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.

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.

ROLE OF OLFACTORY RECEPTOR78 IN CAROTID BODY DEPENDENT SYMPATHETIC ACTIVATION AND HYPERTENSION IN MURINE MODELS OF CHRONIC INTERMITTENT HYPOXIA

2021 ◽  
Author(s):  
Ying-Jie Peng ◽  
Xiaoyu Su ◽  
Benjamin L Wang ◽  
Timothy David Matthews ◽  
Jayasri Nanduri ◽  
...  
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Carotid Body ◽  
Intermittent Hypoxia ◽  
Sensory Nerve ◽  
Chronic Intermittent Hypoxia ◽  
Murine Models ◽  
Nerve Response ◽  
Sympathetic Nervous ◽  
Sympathetic Nerve Activation

Chronic intermittent hypoxia (CIH) is a hallmark manifestation of obstructive sleep apnea (OSA), a widespread breathing disorder. CIH treated rodents exhibit activation of the sympathetic nervous system and hypertension. Heightened carotid body (CB) activity has been implicated in CIH-induced hypertension. CB expresses high abundance of olfactory receptor (Olfr) 78, a G-protein coupled receptor. Olfr 78 null mice exhibit impaired CB sensory nerve response to acute hypoxia. Present study examined whether Olfr78 participates in CB-dependent activation of the sympathetic nervous system and hypertension in CIH treated mice and in hemeoxygenase (HO)-2 null mice experiencing CIH as a consequence of naturally occurring OSA. CIH treated wild type (WT) mice showed hypertension, bio-markers of sympathetic nerve activation, and enhanced CB sensory nerve response to hypoxia and sensory long-term facilitation (sLTF), and these responses were absent in CIH treated Olfr78 null mice. HO-2 null mice showed higher apnea index (AI) (58±1.2 apneas/hour) than WT mice (AI= 8±0.8 apneas/hour), and exhibited elevated blood pressure (BP), plasma NE levels and heightened CB sensory nerve response to hypoxia and sLTF. The magnitude of hypertension correlated with AI in HO-2 null mice. In contrast, HO-2/Olfr78 double null mice showed absence of elevated BP, plasma NE levels, augmented CB response to hypoxia and sLTF. These results demonstrate that Olfr78 participates in sympathetic nerve activation and hypertension, and heightened CB activity in two murine models of CIH.

Correlations of attended and unattended blood pressure with sympathetic nervous system activity in essential hypertension

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
E Manta ◽  
M Kouremeti ◽  
N Kakouri ◽  
A Kasiakogias ◽  
D Konstantinidis ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Essential Hypertension ◽  
Sympathetic Nervous System ◽  
Sympathetic Nerve ◽  
Muscle Sympathetic Nerve Activity ◽  
Left Ventricular ◽  
Hypertensive Group ◽  
Oscillometric Device ◽  
Sympathetic Nervous

Abstract Background/Introduction Measurement of unattended blood pressure (BP) may provide additional information over conventionally attended BP. Moreover, hypertension is related to sympathetic drive while there are scarce data on the diverse links of attended and unattended BP with muscle sympathetic nerve activity (MSNA) in hypertensive patients. Purpose The aim of this study was to appraise the relation of BP levels in the attended and unattended setting with MSNA in patients with essential hypertension. Methods We studied 117 patients with essential hypertension (age: 58±11 years, 60 males, office BP: 142/85±17/10 mmHg, 24-hour BP: 133/80±11/9 mmHg). In all participants sympathetic drive was assessed by MSNA estimations based on established methodology (microneurography). Both unattended BP (patient alone in the room, an oscillometric device programmed to perform 3 BP measurements, at 1-minute intervals, after 5 minutes) and attended BP were measured with the same device, on the same day of MSNA recording, in random order. Patients were divided into the combined attended and unattended hypertensive group when BP≥140/90 mmHg in both attended and unattended BP estimations and to the attended hypertensive group when only attended BP≥140/90 mmHg. Results Patients with combined attended and unattended hypertension (n=70) compared to those with attended hypertension (n=47) did not differ regarding 24-h ambulatory BP levels, glucose levels, renal function and left ventricular mass index (p=NS for all). Moreover, patients with combined attended and unattended hypertension compared to those with attended hypertension were characterized by greater levels of MSNA (43.7±9.9 vs 37.7±9.7 bursts per minute, p=0.032). In all participants, sympathetic nerve traffic as assessed by resting MSNA was related to attended systolic BP (r=0.270, p=0.003), attended diastolic BP (r=0.344, p=0.001), unattended systolic BP (r=0.263, p=0.004) and unattended diastolic BP (r=0.274, p=0.003). Conclusions The phenotype of combined attended and unattended hypertension compared to attended hypertension is accompanied by higher sympathetic nervous system activation. Moreover, the close association of MSNA with attended and unattended BP levels in essential hypertension, further supports the key role of sympathetic drive in modulating BP. Funding Acknowledgement Type of funding source: None

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