Regional and functional differences in the distribution of vestibulosympathetic reflexes

1998 ◽  
Vol 275 (3) ◽  
pp. R824-R835 ◽  
Author(s):  
I. A. Kerman ◽  
B. J. Yates
Keyword(s):  
Blood Pressure ◽  
Vestibular System ◽  
Sympathetic Nerves ◽  
Relative Magnitude ◽  
External Carotid ◽  
Sympathetic Outflow ◽  
Renal Nerve ◽  
Body Regions ◽  
Sympathetic Efferents ◽  
Vestibulosympathetic Reflexes

Although considerable evidence suggests that the vestibular system regulates sympathetic outflow during movement and changes in posture, little is known about relative vestibular influences on activity of different sympathetic nerves and sympathetic efferents with different functions. In the present study, we demonstrated that electrical stimulation of the vestibular nerve in the cat elicited responses in sympathetic nerves innervating the head and abdominal viscera. This observation suggests that activity of sympathetic efferents innervating multiple body regions is affected by vestibular signals. These responses were attenuated by >80% when blood pressure was increased to >160 mmHg. Because raising blood pressure decreases the responsiveness of vasoconstrictor fibers, the simplest explanation for these data is that the vestibular system provides particularly strong inputs to components of the sympathetic nervous system that regulate peripheral vascular resistance. Furthermore, the relative magnitude of vestibulosympathetic reflexes was over four times larger in one sympathetic nerve composed mainly of vasoconstrictor efferents (renal nerve) than another nerve (external carotid nerve) containing similar types of fibers. Collectively, these data indicate that the vestibular system has selective influences on sympathetic outflow to particular tissues and body regions.

Contrasting reflexes evoked by chemical activation of cardiac afferent nerves

1980 ◽  
Vol 239 (3) ◽  
pp. H316-H325 ◽  
Author(s):  
K. A. Reimann ◽  
L. C. Weaver
Keyword(s):  
Potassium Chloride ◽  
Chemical Activation ◽  
Sympathetic Nerves ◽  
Sympathetic Outflow ◽  
Afferent Neurons ◽  
Renal Nerve ◽  
Afferent Nerves ◽  
Excitatory Responses ◽  
Upper Thoracic ◽  
Arterial Baroreceptor

Afferent neurons within cardiac sympathetic nerves can reflexly excite central sympathetic outflow. However, their contribution to cardiovascular control remains unclear because they are potentially opposed by inhibitory reflexes of cardiac vagal or arterial baroreceptor afferent origin. It was considered that sympathetically mediated, excitatory responses might be more prominent when initiated by chemical stimulation. In chloralose-anesthetized, vagotomized, sinoaortic-denervated cats, epicardial or intracoronary administration of bradykinin or potassium chloride evoked renal nerve excitation and pressor responses mediated by cardiac sympathetic afferent nerves. When upper thoracic sympathetic nerves were severed, and vagal afferent nerves remained intact, bradykinin and potassium chloride produced inhibition of renal nerve activity and depressor responses. When sympathetic and vagal components of cardiac innervation remained intact, these substances produced excitation, inhibition, or no change in sympathetic outflow. Excitation occurred as often as inhibition. A similar pattern was observed when arterial baroreceptor nerves remained intact. These data illustrate that cardiac sympathetic afferent neurons can have significant excitatory influences on the cardiovascular system in spite of opposition by inhibitory afferent groups.

scholarly journals Hypertension Associated with Fructose and High Salt: Renal and Sympathetic Mechanisms

Nutrients ◽  
2019 ◽  
Vol 11 (3) ◽  
pp. 569 ◽  
Author(s):  
Dragana Komnenov ◽  
Peter Levanovich ◽  
Noreen Rossi
Keyword(s):  
Blood Pressure ◽  
Chronic Renal Disease ◽  
Sympathetic Nerves ◽  
Renal Nerve ◽  
Renin Angiotensin Aldosterone System ◽  
Renin Angiotensin ◽  
Salt Consumption ◽  
High Fructose ◽  
Salt Sensitive Hypertension ◽  
Renal Sympathetic

Hypertension is a leading cause of cardiovascular and chronic renal disease. Despite multiple important strides that have been made in our understanding of the etiology of hypertension, the mechanisms remain complex due to multiple factors, including the environment, heredity and diet. This review focuses on dietary contributions, providing evidence for the involvement of elevated fructose and salt consumption that parallels the increased incidence of hypertension worldwide. High fructose loads potentiate salt reabsorption by the kidney, leading to elevation in blood pressure. Several transporters, such as NHE3 and PAT1 are modulated in this milieu and play a crucial role in salt-sensitivity. High fructose ingestion also modulates the renin-angiotensin-aldosterone system. Recent attention has been shifted towards the contribution of the sympathetic nervous system, as clinical trials demonstrated significant reductions in blood pressure following renal sympathetic nerve ablation. New preclinical data demonstrates the activation of the renal sympathetic nerves in fructose-induced salt-sensitive hypertension, and reductions of blood pressure after renal nerve ablation. This review further demonstrates the interplay between sodium handling by the kidney, the renin-angiotensin-aldosterone system, and activation of the renal sympathetic nerves as important mechanisms in fructose and salt-induced hypertension.

Patterning of somatosympathetic reflexes

1999 ◽  
Vol 277 (3) ◽  
pp. R716-R724 ◽  
Author(s):  
I. A. Kerman ◽  
B. J. Yates
Keyword(s):  
Nerve Stimulation ◽  
Sympathetic Nerve ◽  
Vestibular Stimulation ◽  
Specific Pattern ◽  
External Carotid ◽  
Renal Nerve ◽  
Muscle Afferent ◽  
Somatosympathetic Responses ◽  
Sympathetic Nerve Activation ◽  
Vestibulosympathetic Reflexes

In a previous study, we reported that vestibular nerve stimulation in the cat elicits a specific pattern of sympathetic nerve activation, such that responses are particularly large in the renal nerve. This patterning of vestibulosympathetic reflexes was the same in anesthetized and decerebrate preparations. In the present study, we report that inputs from skin and muscle also elicit a specific patterning of sympathetic outflow, which is distinct from that produced by vestibular stimulation. Renal, superior mesenteric, and lumbar colonic nerves respond most strongly to forelimb and hindlimb nerve stimulation (∼60% of maximal nerve activation), whereas external carotid and hypogastric nerves were least sensitive to these inputs (∼20% of maximal nerve activation). In contrast to vestibulosympathetic reflexes, the expression of responses to skin and muscle afferent activation differs in decerebrate and anesthetized animals. In baroreceptor-intact animals, somatosympathetic responses were strongly attenuated (to <20% of control in every nerve) by increasing blood pressure levels to >150 mmHg. These findings demonstrate that different types of somatic inputs elicit specific patterns of sympathetic nerve activation, presumably generated through distinct neural circuits.

Cardiovascular and renal nerve responses to static muscle contraction of decerebrate rabbits

1994 ◽  
Vol 77 (5) ◽  
pp. 2449-2455 ◽  
Author(s):  
L. B. Wilson ◽  
C. K. Dyke ◽  
J. A. Pawelczyk ◽  
P. T. Wall ◽  
J. H. Mitchell
Keyword(s):  
Blood Pressure ◽  
Muscle Contraction ◽  
Arterial Blood Pressure ◽  
Triceps Surae ◽  
Sympathetic Outflow ◽  
Subsequent Increase ◽  
Renal Nerve ◽  
Arterial Blood ◽  
Initial Decrease ◽  
Blood Pressure Responses

The purpose of this study was to determine whether the biphasic arterial blood pressure responses elicited by static muscle contraction of decerebrate rabbits are mediated, at least in part, by an initial decrease and a subsequent increase in sympathetic outflow. Renal sympathetic nerve activity (RSNA) was used as an index of sympathetic outflow. Static contraction of the triceps surae muscle (n = 14) initially decreased mean arterial blood pressure (MAP) -20 +/- 3 mmHg and heart rate (HR) -15 +/- 5 beats/min (nadir values). After this initial decrease, MAP increased 12 +/- 2 mmHg (peak increase) above baseline and there was a tendency for HR to be elevated (6 +/- 3 beats/min). The changes in RSNA during muscle contraction (n = 6) mirrored the nadir and peak responses of MAP (-50 +/- 9 and 32 +/- 11%). Muscle stretch (n = 11) also evoked similar nadir and peak responses of MAP (-20 +/- 5 and 9 +/- 1 mmHg), HR (-17 +/- 7 and 3 +/- 3 beats/min), and RSNA (-43 +/- 9 and 46 +/- 15%). These data suggest that the initial depressor and subsequent pressor responses elicited by skeletal muscle contraction and stretch are mediated, at least in part, by biphasic changes in sympathetic outflow.

scholarly journals Renal Denervation by Noninvasive Stereotactic Radiotherapy Induces Persistent Reduction of Sympathetic Activity in a Hypertensive Swine Model

2021 ◽  
Author(s):  
Xingxing Cai ◽  
Yichen Shen ◽  
Yuli Yang ◽  
Wei Wang ◽  
Li Qian ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Nerve Regeneration ◽  
Nerve Injury ◽  
Sympathetic Activity ◽  
Renal Denervation ◽  
Blood Pressure Response ◽  
Sympathetic Nerves ◽  
Swine Model ◽  
Renal Nerve ◽  
Deoxycorticosterone Acetate

Background We have previously reported the feasibility of noninvasive stereotactic body radiotherapy (SBRT) as a novel approach for renal denervation. Methods and Results Herein, from a translational point of view, we assessed the antihypertensive effect and chronological evolution of SBRT‐induced renal nerve injury within 6 months in a hypertensive swine model. Hypertension was induced in swine by subcutaneous implantation of deoxycorticosterone acetate pellets in combination with a high‐salt diet. A single dose of 25 Gy with SBRT was delivered for renal denervation in 9 swine within 3.4±1.0 minutes. Blood pressure levels at baseline and 1 and 6 months post‐SBRT were comparable to control (n=5), whereas renal norepinephrine was significantly lower at 6 months ( P <0.05). Abdominal computed tomography, performed before euthanasia and renal function assessment, remained normal. Standard semiquantitative histological assessment showed that compared with control (1.4±0.4), renal nerve injury was greater at 1 month post‐SBRT (2.3±0.3) and peaked at 6 months post‐SBRT (3.2±0.8) ( P <0.05), along with a higher proportion of active caspase‐3–positive nerves ( P <0.05). Moreover, SBRT resulted in continuous dysfunction of renal sympathetic nerves and low level of nerve regeneration in 6 months by immunohistochemistry analysis. Conclusions SBRT delivering 25 Gy for renal denervation was safe and related to sustained reduction of sympathetic activity by aggravating nerve damage and inhibiting nerve regeneration up to 6 months; however, its translation to clinical trial should be cautious because of the negative blood pressure response in the deoxycorticosterone acetate–salt hypertensive swine model.

Effect of in vivo gene transfer of nNOS in the PVN on renal nerve discharge in rats

2002 ◽  
Vol 282 (2) ◽  
pp. H594-H601 ◽  
Author(s):  
Yi-Fan Li ◽  
Shyamal K. Roy ◽  
Keith M. Channon ◽  
Irving H. Zucker ◽  
Kaushik P. Patel
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Nadph Diaphorase ◽  
Sympathetic Outflow ◽  
Renal Nerve ◽  
Cultured Fibroblasts ◽  
Dose Dependent Increase ◽  
Nerve Discharge

The paraventricular nucleus (PVN) of the hypothalamus is known to be involved in the control of sympathetic outflow. Nitric oxide (NO) has been shown to have a sympathoinhibitory effect in the PVN. The goal of the present study was to examine the influence of overexpression of neuronal NO synthase (nNOS) within the PVN on renal sympathetic nerve discharge (RSND). Adenovirus vectors encoding either nNOS (Ad.nNOS) or β-galactosidase (Ad.β-Gal) were transfected into the PVN in vivo. Initially, the dose of adenovirus needed for infection was determined from in vitro infection of cultured fibroblasts. In Ad.nNOS-treated rats, the local expression of nNOS within the PVN was confirmed by histochemistry for NADPH-diaphorase-positive neurons. There was a robust increase in staining of NADPH-diaphorase-positive cells in the PVN on the side injected with Ad.nNOS. The staining peaked at 3 days after injection of the virus. In α-chloralose- and urethane-anesthetized rats, microinjection of N G-monomethyl-l-arginine (l-NMMA), a NO antagonist, into the PVN produced a dose-dependent increase in RSND, blood pressure, and heart rate. There was a potentiation of the increase in RSND, blood pressure, and heart rate due to l-NMMA in Ad.nNOS-injected rats compared with Ad.β-Gal-injected rats. These results suggest that the endogenous NO-mediated effect in the PVN of Ad.nNOS-treated rats is more effective in suppressing RSND compared with Ad.β-Gal-treated rats. These observations support the contention that an overexpression of nNOS within the PVN may be responsible for increased suppression of sympathetic outflow. This technique may be useful in pathological conditions know to have increased sympathetic outflow, such as hypertension or heart failure.

Sympathetic nerve discharge in chronic spinal cat

1982 ◽  
Vol 243 (3) ◽  
pp. H463-H470 ◽  
Author(s):  
J. L. Ardell ◽  
S. M. Barman ◽  
G. L. Gebber
Keyword(s):  
Blood Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerves ◽  
Slow Waves ◽  
External Carotid ◽  
Spinal Transection ◽  
Reflex Mechanism ◽  
Ganglionic Blockade ◽  
Spinal Segments ◽  
Nerve Discharge

A study was made of external carotid, renal, and splanchnic sympathetic nerve discharge (SND) in chloralose-anesthetized cats subjected to transection of the sixth cervical spinal segment 2-37 days earlier. Minimal activity was observed under normocapnic conditions 2 days after spinal transection, and ganglionic blockade failed to lower blood pressure. Moderate hypercapnia increased SND and led to synchronization of activity into 1-6 cycle/s slow waves. Such slow-wave activity was present under normocapnic conditions in cats 9-37 days after spinal transection. Ganglionic blockade significantly reduced blood pressure in these preparations. The interval between successive 1-6 cycle/s slow waves was variable. Thus, unlike the case in baroreceptor-denervated cats with an intact neuraxis [Barman and Gebber, Am. J. Physiol. 239 (Regulatory Integrative Comp. Physiol. 8): R42-R47, 1980], chronic spinal cats are incapable of rhythm generation in the 1-6 cycle/s frequency range. Crosscorrelation analysis revealed that the discharges of pairs of segmental (but not intersegmental) sympathetic nerves were related in the chronic spinal cat. This situation differs from that in the baroreceptor-denervated cat in which the discharges of pairs of intersegmental as well as segmental sympathetic nerves are related. Thus coordination of activity in sympathetic nerves that arise from different spinal segments requires the integrity of bulbospinal connections. Finally, no evidence was obtained for the existence of a baroreceptor-like reflex mechanism acting to control SND in the chronic spinal cat.

Effect of angiotensin II receptor blockade on autonomic nervous system function in patients with essential hypertension

2006 ◽  
Vol 290 (4) ◽  
pp. H1706-H1712 ◽  
Author(s):  
Henry Krum ◽  
Elisabeth Lambert ◽  
Emma Windebank ◽  
Duncan J. Campbell ◽  
Murray Esler
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Essential Hypertension ◽  
Sympathetic Nerves ◽  
Whole Body ◽  
Sympathetic Outflow ◽  
Norepinephrine Release ◽  
Sympathetic Nervous ◽  
Central Sympathetic Outflow ◽  
Norepinephrine Spillover

It has long been proposed that the renin-angiotensin system exerts a stimulatory influence on the sympathetic nervous system, including augmentation of central sympathetic outflow and presynaptic facilitation of norepinephrine release from sympathetic nerves. We tested this proposition in 19 patients with essential hypertension, evaluating whether the angiotensin receptor blockers (ARBs) eprosartan and losartan had identifiable antiadrenergic properties. This was done in a prospective, randomized, three-way placebo-controlled study of crossover design. Patients were randomized to 600 mg of eprosartan daily, 50 mg of losartan daily, or placebo. The treatment period was 4 wk, with 2-wk washout periods. Multiunit firing rates in efferent sympathetic nerves distributed to skeletal muscle vasculature (muscle sympathetic nerve activity, MSNA) were measured with microneurography, testing whether ARBs inhibit central sympathetic outflow. In parallel, isotope dilution methodology was used to measure whole body norepinephrine spillover to plasma. Mean blood pressure on placebo was 151/98 mmHg, with both ARBs causing reductions of ∼11 mmHg systolic and 6 mmHg diastolic pressure, placebo corrected. Both MSNA [35 ± 12 bursts/min (mean ± SD) on placebo] and whole body norepinephrine spillover [366 ± 247 ng/min] were unchanged by ARB administration, indicating that the ARBs did not materially inhibit central sympathetic outflow or act presynaptically to reduce norepinephrine release at existing rates of nerve firing. These findings contrast with the easily demonstrable reduction in sympathetic nervous activity produced by antihypertensive drugs of the imidazoline-binding class, which are known to act within the brain to inhibit sympathetic nervous outflow. We conclude that sympathetic nervous inhibition is not a major component of the blood pressure-lowering action of ARBs in essential hypertension.

Defenselike patterns of spinal sympathetic outflow involving the 10-Hz and cardiac-related rhythms

2000 ◽  
Vol 278 (6) ◽  
pp. R1616-R1626 ◽  
Author(s):  
Gerard L. Gebber ◽  
Sheng Zhong ◽  
Craig Lewis ◽  
Susan M. Barman
Keyword(s):  
Blood Pressure ◽  
Time Domain ◽  
Sympathetic Nerve ◽  
High Frequency ◽  
Control Level ◽  
Sympathetic Nerves ◽  
Sympathetic Outflow ◽  
Related Activity ◽  
Free Running ◽  
Stimulation Of

Frequency- and time-domain analyses were used to compare the effects of stimulation of the defense region of the midbrain periaqueductal gray (PAG) on the 10-Hz and cardiac-related discharges of sympathetic nerves with different cardiovascular targets. In baroreceptor-denervated cats anesthetized with urethan, PAG stimulation at frequencies equal to or higher (up to 25 Hz) than that of the free-running 10-Hz rhythm produced an immediate and sustained decrease in vertebral sympathetic nerve (VN) 10-Hz activity but increased the 10-Hz discharges of the inferior cardiac (CN) and renal (RN) nerves. In baroreceptor-innervated cats, VN cardiac-related activity was initially unchanged by high-frequency (25-Hz) PAG stimulation, or it increased along with that in the CN and RN. Later, during high-frequency PAG stimulation, when the rise in blood pressure approached its peak, VN cardiac-related activity usually was reduced below control level. At this time, the increases in CN and RN cardiac-related discharges were largely sustained. The cardiac-related discharges of the three nerves were unaffected by PAG stimulation at frequencies just below or just above that of the heartbeat. We conclude that the defenselike pattern of spinal sympathetic outflow involving the 10-Hz rhythm is different in mechanism and character from that involving the cardiac-related rhythm.

scholarly journals Sympathetic Enhancement of Memory T-Cell Homing and Hypertension Sensitization

2020 ◽  
Vol 126 (6) ◽  
pp. 708-721 ◽  
Author(s):  
Liang Xiao ◽  
Luciana Simao do Carmo ◽  
Jason D. Foss ◽  
Wei Chen ◽  
David G. Harrison
Keyword(s):  
Bone Marrow ◽  
T Cells ◽  
T Cell ◽  
Sympathetic Nerves ◽  
Designer Drug ◽  
Effector Memory ◽  
Bone Marrow Niche ◽  
Sympathetic Outflow ◽  
Ang Ii ◽  
Cell Homing

Rationale: Effector memory T lymphocytes (T EM cells) exacerbate hypertension in response to repeated hypertensive stimuli. These cells reside in the bone marrow for prolonged periods and can be reactivated on reexposure to the hypertensive stimulus. Objective: Because hypertension is associated with increased sympathetic outflow to the bone marrow, we hypothesized that sympathetic nerves regulate accumulation and reactivation of bone marrow–residing hypertension-specific T EM cells. Methods and Results: Using unilateral superior cervical ganglionectomy in wild-type C57BL/6 mice, we showed that sympathetic nerves create a bone marrow environment that supports residence of hypertension-specific CD8 + T cells. These cells, defined by their proliferative response on coculture with dendritic cells from Ang (angiotensin) II–infused mice, were reduced in denervated compared with innervated bone of Ang II–infused mice. Adoptively transferred CD8 + T cells from Ang II–infused mice preferentially homed to innervated compared with denervated bone. In contrast, ovalbumin responsive T cells from OT-I mice did not exhibit this preferential homing. Increasing superior cervical ganglion activity by activating Gq-coupled designer receptor exclusively activated by designer drug augmented CD8 + T EM bone marrow accumulation. Adoptive transfer studies using mice lacking β2AR (β2 adrenergic receptors) indicate that β2AR in the bone marrow niche, rather than T-cell β2AR is critical for T EM cell homing. Inhibition of global sympathetic outflow using Gi-coupled DREADD (designer receptor exclusively activated by designer drug) injected into the rostral ventrolateral medulla or treatment with a β2AR antagonist reduced hypertension-specific CD8 + T EM cells in the bone marrow and reduced the hypertensive response to a subsequent response to low dose Ang II. Conclusions: Sympathetic nerves contribute to the homing and survival of hypertension-specific T EM cells in the bone marrow after they are formed in hypertension. Inhibition of sympathetic nerve activity and β2AR blockade reduces these cells and prevents the blood pressure elevation and renal inflammation on reexposure to hypertension stimuli.

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