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Journal articles on the topic 'Sympathetic pathway'

Author: Grafiati

Published: 3 June 2025

Last updated: 31 July 2025

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1

Philpott, Karen L., Mary Jane McCarthy, Anke Klippel, and Lee L. Rubin. "Activated Phosphatidylinositol 3-Kinase and Akt Kinase Promote Survival of Superior Cervical Neurons." Journal of Cell Biology 139, no. 3 (1997): 809–15. http://dx.doi.org/10.1083/jcb.139.3.809.

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The signaling pathways that mediate the ability of NGF to support survival of dependent neurons are not yet completely clear. However previous work has shown that the c-Jun pathway is activated after NGF withdrawal, and blocking this pathway blocks neuronal cell death. In this paper we show that over-expression in sympathetic neurons of phosphatidylinositol (PI) 3-kinase or its downstream effector Akt kinase blocks cell death after NGF withdrawal, in spite of the fact that the c-Jun pathway is activated. Yet, neither the PI 3-kinase inhibitor LY294002 nor a dominant negative PI 3-kinase cause

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2

Gabor, Alexander, and Frans H. H. Leenen. "Central neuromodulatory pathways regulating sympathetic activity in hypertension." Journal of Applied Physiology 113, no. 8 (2012): 1294–303. http://dx.doi.org/10.1152/japplphysiol.00553.2012.

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The classical neurotransmitters, glutamate and GABA, mediate fast (milliseconds) synaptic transmission and modulate its effectiveness through slow (seconds to minutes) signaling processes. Angiotensinergic pathways, from the lamina terminalis to the paraventricular nucleus (PVN)/supraoptic nucleus and rostral ventrolateral medulla (RVLM), are activated by stimuli such as circulating angiotensin type II (Ang II), cerebrospinal fluid (CSF) sodium ion concentration ([Na+]), and possibly plasma aldosterone, leading to sympathoexcitation, largely by decreasing GABA and increasing glutamate release.

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3

Nakade, Yukiomi, Daisuke Tsuchida, Hiroyuki Fukuda, Masahiro Iwa, Theodore N. Pappas, and Toku Takahashi. "Restraint stress delays solid gastric emptying via a central CRF and peripheral sympathetic neuron in rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 288, no. 2 (2005): R427—R432. http://dx.doi.org/10.1152/ajpregu.00499.2004.

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Central corticotropin-releasing factor (CRF) delays gastric emptying through the autonomic nervous system. CRF plays an important role in mediating delayed gastric emptying induced by stress. However, it is not clear whether a sympathetic or parasympathetic pathway is involved in the mechanism of central CRF-induced inhibition of solid gastric emptying. The purpose of this study was to investigate whether 1) CRF inhibits solid gastric emptying via a peripheral sympathetic pathway and 2) stress-induced inhibition of solid gastric emptying is mediated via a central CRF and peripheral sympathetic

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4

Leenen, Frans H. H., Mordecai P. Blaustein, and John M. Hamlyn. "Update on angiotensin II: new endocrine connections between the brain, adrenal glands and the cardiovascular system." Endocrine Connections 6, no. 7 (2017): R131—R145. http://dx.doi.org/10.1530/ec-17-0161.

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In the brain, angiotensinergic pathways play a major role in chronic regulation of cardiovascular and electrolyte homeostasis. Increases in plasma angiotensin II (Ang II), aldosterone, [Na+] and cytokines can directly activate these pathways. Chronically, these stimuli also activate a slow neuromodulatory pathway involving local aldosterone, mineralocorticoid receptors (MRs), epithelial sodium channels and endogenous ouabain (EO). This pathway increases AT1R and NADPH oxidase subunits and maintains/further increases the activity of angiotensinergic pathways. These brain pathways not only incre

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5

Westcott, Katherine V., Bing S. Huang, and Frans H. H. Leenen. "Brain renin–angiotensin–aldosterone system and ventricular remodeling after myocardial infarct: a reviewThis article is one of a selection of papers published in a special issue on Advances in Cardiovascular Research." Canadian Journal of Physiology and Pharmacology 87, no. 12 (2009): 979–88. http://dx.doi.org/10.1139/y09-067.

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After a myocardial infarct (MI), a variety of mechanisms contribute to progressive cardiac remodeling and dysfunction. Progressive activation of central sympathoexcitatory pathways appears to depend on a neuromodulatory pathway, involving local production of aldosterone and release of endogenous ouabain-like compounds (‘ouabain’) possibly from magnocellular neurons in the supraoptic and paraventricular nuclei. ‘Ouabain’ may lower the membrane potential of neurons and thereby enhance activity of angiotensinergic pathways. These central pathways appear to coordinate progressive activation of sev

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6

CHOWDHARY, Saqib, and Jonathan N. TOWNEND. "Role of nitric oxide in the regulation of cardiovascular autonomic control." Clinical Science 97, no. 1 (1999): 5–17. http://dx.doi.org/10.1042/cs0970005.

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Alteration in function of the cardiac autonomic nervous system has proved to be a powerful predictor of cardiac death or serious arrhythmia in patients with cardiac disease, yet little is known about the mechanisms by which this system is regulated. Recent evidence suggests that the gaseous molecule nitric oxide (NO) may act as an important mediator in this pathway. Histochemical staining techniques have identified neuronal populations that contain NO synthase within medullary cardio-regulatory sites and their peripheral autonomic pathways. Drugs that modulate the NO pathway (administered both

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7

Molinas, Adrien J. R., Lucie D. Desmoulins, Roslyn K. Davis, et al. "High-Fat Diet Modulates the Excitability of Neurons within the Brain–Liver Pathway." Cells 12, no. 8 (2023): 1194. http://dx.doi.org/10.3390/cells12081194.

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Stimulation of hepatic sympathetic nerves increases glucose production and glycogenolysis. Activity of pre-sympathetic neurons in the paraventricular nucleus (PVN) of the hypothalamus and in the ventrolateral and ventromedial medulla (VLM/VMM) largely influence the sympathetic output. Increased activity of the sympathetic nervous system (SNS) plays a role in the development and progression of metabolic diseases; however, despite the importance of the central circuits, the excitability of pre-sympathetic liver-related neurons remains to be determined. Here, we tested the hypothesis that the act

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8

Faraci, F. M., M. G. Motley, and D. D. Heistad. "Activation of a cranial vasodilator pathway during seizures in rats." American Journal of Physiology-Heart and Circulatory Physiology 251, no. 5 (1986): H969—H975. http://dx.doi.org/10.1152/ajpheart.1986.251.5.h969.

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The purpose of this study was to determine whether seizures, which activate sympathetic nerves, also activate a vasodilator pathway to extracranial tissues of the head. Blood flow was measured with microspheres during control conditions and seizures in anesthetized, paralyzed rats. Seizures were produced by bicuculline or pentylenetetrazole. During seizures in rats with intact sympathetic nerves, blood flow to masseter muscle decreased and blood flow to tongue did not change. Following bilateral cervical sympathetic denervation or high spinal cord section, seizure produced marked increases in

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9

Li, Zhixiao, Yujuan Li, Zhigang He, Zhen Li, Weiguo Xu, and HongBing Xiang. "The Preventive Effect of Cardiac Sympathetic Denervation Induced by 6-OHDA on Myocardial Ischemia–Reperfusion Injury: The Changes of lncRNA/circRNAs-miRNA-mRNA Network of the Upper Thoracic Spinal Cord in Rats." Oxidative Medicine and Cellular Longevity 2021 (November 29, 2021): 1–28. http://dx.doi.org/10.1155/2021/2492286.

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In this study, we investigated whether chemical 6-hydroxydopamine (6-OHDA) stimuli caused cardiac sympathetic denervation (SD), and we analyzed gene expression profiles to determine the changes in the lncRNA/circRNAs-miRNA-mRNA network in the affected spinal cord segments to identify putative target genes and molecular pathways in rats with myocardial ischemia–reperfusion injury (MIRI). Our results showed that cardiac sympathetic denervation induced by 6-OHDA alleviated MIRI. Compared with the ischemia reperfusion (IR, MIRI model) group, there were 148 upregulated and 51 downregulated mRNAs, 1

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10

Aloyz, Raquel S., Shernaz X. Bamji, Christine D. Pozniak, et al. "P53 Is Essential for Developmental Neuron Death as Regulated by the TrkA and p75 Neurotrophin Receptors." Journal of Cell Biology 143, no. 6 (1998): 1691–703. http://dx.doi.org/10.1083/jcb.143.6.1691.

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Naturally occurring sympathetic neuron death is the result of two apoptotic signaling events: one normally suppressed by NGF/TrkA survival signals, and a second activated by the p75 neurotrophin receptor. Here we demonstrate that the p53 tumor suppressor protein, likely as induced by the MEKK-JNK pathway, is an essential component of both of these apoptotic signaling cascades. In cultured neonatal sympathetic neurons, p53 protein levels are elevated in response to both NGF withdrawal and p75NTR activation. NGF withdrawal also results in elevation of a known p53 target, the apoptotic protein Ba

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11

Feinberg, Konstantin, Adelaida Kolaj, Chen Wu, et al. "A neuroprotective agent that inactivates prodegenerative TrkA and preserves mitochondria." Journal of Cell Biology 216, no. 11 (2017): 3655–75. http://dx.doi.org/10.1083/jcb.201705085.

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Axon degeneration is an early event and pathological in neurodegenerative conditions and nerve injuries. To discover agents that suppress neuronal death and axonal degeneration, we performed drug screens on primary rodent neurons and identified the pan-kinase inhibitor foretinib, which potently rescued sympathetic, sensory, and motor wt and SOD1 mutant neurons from trophic factor withdrawal-induced degeneration. By using primary sympathetic neurons grown in mass cultures and Campenot chambers, we show that foretinib protected neurons by suppressing both known degenerative pathways and a new pa

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12

Holstein, Gay R., Giorgio P. Martinelli, and Victor L. Friedrich. "Anatomical observations of the caudal vestibulo-sympathetic pathway." Journal of Vestibular Research 21, no. 1 (2011): 49–62. http://dx.doi.org/10.3233/ves-2011-0395.

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13

Nakamura, Kazuhiro, and Shaun F. Morrison. "A thermosensory pathway controlling sympathetic and shivering thermogenesis." Autonomic Neuroscience 135, no. 1-2 (2007): 27. http://dx.doi.org/10.1016/j.autneu.2007.06.023.

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14

Holstein, Gay R., Victor L. Friedrich, and Giorgio P. Martinelli. "Imidazoleacetic acid-ribotide in vestibulo-sympathetic pathway neurons." Experimental Brain Research 234, no. 10 (2016): 2747–60. http://dx.doi.org/10.1007/s00221-016-4725-2.

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15

Holstein, Gay R., Victor L. Friedrich, and Giorgio P. Martinelli. "Projection neurons of the vestibulo-sympathetic reflex pathway." Journal of Comparative Neurology 522, no. 9 (2014): 2053–74. http://dx.doi.org/10.1002/cne.23517.

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16

Putcha, Girish V., Charles A. Harris, Krista L. Moulder, Rachael M. Easton, Craig B. Thompson, and Eugene M. Johnson. "Intrinsic and extrinsic pathway signaling during neuronal apoptosis." Journal of Cell Biology 157, no. 3 (2002): 441–53. http://dx.doi.org/10.1083/jcb.200110108.

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Trophic factor deprivation (TFD)-induced apoptosis in sympathetic neurons requires macromolecular synthesis–dependent BAX translocation, cytochrome c (cyt c) release, and caspase activation. Here, we report the contributions of other intrinsic and extrinsic pathway signals to these processes. Sympathetic neurons expressed all antiapoptotic BCL-2 proteins examined, yet expressed only certain BH3-only and multidomain proapoptotic BCL-2 family members. All coexpressed proapoptotic proteins did not, however, exhibit functional redundancy or compensatory expression, at least in the Bax−/−, Bak−/−,

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17

Ernsberger, Uwe, Thomas Deller, and Hermann Rohrer. "The diversity of neuronal phenotypes in rodent and human autonomic ganglia." Cell and Tissue Research 382, no. 2 (2020): 201–31. http://dx.doi.org/10.1007/s00441-020-03279-6.

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Abstract Selective sympathetic and parasympathetic pathways that act on target organs represent the terminal actors in the neurobiology of homeostasis and often become compromised during a range of neurodegenerative and traumatic disorders. Here, we delineate several neurotransmitter and neuromodulator phenotypes found in diverse parasympathetic and sympathetic ganglia in humans and rodent species. The comparative approach reveals evolutionarily conserved and non-conserved phenotypic marker constellations. A developmental analysis examining the acquisition of selected neurotransmitter properti

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18

Yu, Li-Ying, Eija Jokitalo, Yun-Fu Sun, et al. "GDNF-deprived sympathetic neurons die via a novel nonmitochondrial pathway." Journal of Cell Biology 163, no. 5 (2003): 987–97. http://dx.doi.org/10.1083/jcb.200305083.

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The mitochondrial death pathway is triggered in cultured sympathetic neurons by deprivation of nerve growth factor (NGF), but the death mechanisms activated by deprivation of other neurotrophic factors are poorly studied. We compared sympathetic neurons deprived of NGF to those deprived of glial cell line–derived neurotrophic factor (GDNF). In contrast to NGF-deprived neurons, GDNF-deprived neurons did not die via the mitochondrial pathway. Indeed, cytochrome c was not released to the cytosol; Bax and caspase-9 and -3 were not involved; overexpressed Bcl-xL did not block the death; and the mit

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19

Cui, Shuai, Yiping Zhou, Shengbing Wu, Jian Cao, Guoqi Zhu, and Meiqi Zhou. "Electroacupuncture Improved the Function of Myocardial Ischemia Involved in the Hippocampus-Paraventricular Nucleus-Sympathetic Nerve Pathway." Evidence-Based Complementary and Alternative Medicine 2018 (2018): 1–13. http://dx.doi.org/10.1155/2018/2870676.

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We investigated the hippocampus-paraventricular nucleus- (PVN-) sympathetic nerve pathway in electroacupuncture (EA) at the heart meridian for the treatment of myocardial ischemia by observing PVN neuronal discharge, sympathetic nerve discharge, and hemodynamics parameters. Sprague Dawley (SD) rats were equally divided into four groups: Sham, Model, Model + EA, and Model + EA + Lesion. The model rat was established by ligating the left anterior descending branch of the coronary artery. Changes in the sympathetic nerve discharge and hemodynamic parameters were observed. The Model + EA exhibited

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20

Dai, Xiaoling, Xian Cao, and David L. Kreulen. "Superoxide anion is elevated in sympathetic neurons in DOCA-salt hypertension via activation of NADPH oxidase." American Journal of Physiology-Heart and Circulatory Physiology 290, no. 3 (2006): H1019—H1026. http://dx.doi.org/10.1152/ajpheart.00052.2005.

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Superoxide anion (O2−·) production is elevated in sympathetic ganglion neurons and in the vasculature of hypertensive animals; however, it is not known what enzymatic pathway(s) are responsible for O2−· production. To determine the pathway(s) of O2−· production in sympathetic neurons, we examined the presence of mRNA of NADPH oxidase subunits in sympathetic ganglionic neurons and differentiated PC-12 cells. The mRNAs for NADPH oxidase subunits p47 phox, p22 phox, gp91 phox, and NOX1 were present in sympathetic neurons and PC-12 cells, whereas the NOX4 homologue was present in sympathetic neuro

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21

Rathner, Joseph A., Christopher J. Madden, and Shaun F. Morrison. "Central pathway for spontaneous and prostaglandin E2-evoked cutaneous vasoconstriction." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 295, no. 1 (2008): R343—R354. http://dx.doi.org/10.1152/ajpregu.00115.2008.

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A reduction of heat loss to the environment through increased cutaneous vasoconstrictor (CVC) sympathetic outflow contributes to elevated body temperature during fever. We determined the role of neurons in the dorsomedial hypothalamus (DMH) in increases in CVC sympathetic tone evoked by PGE2 into the preoptic area (POA) in chloralose/urethane-anesthetized rats. The frequency of axonal action potentials of CVC sympathetic ganglion cells recorded from the surface of the tail artery was increased by 1.8 Hz following nanoinjections of bicuculline (50 pmol) into the DMH. PGE2 nanoinjection into the

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22

Oikawa, Susumu, Kyutaro Kawagishi, Kumiko Yokouchi, Nanae Fukushima, and Tetsuji Moriizumi. "Immunohistochemical determination of the sympathetic pathway in the orbit via the cranial nerves in humans." Journal of Neurosurgery 101, no. 6 (2004): 1037–44. http://dx.doi.org/10.3171/jns.2004.101.6.1037.

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Object. The present study was undertaken to elucidate the extent and precise distribution of the postganglionic sympathetic fibers in the cranial nerves projecting to the orbit and to reconstruct sympathetic routes in the orbit in humans. For this purpose, the authors made an immunohistochemical determination of the sympathetic fibers by using an antibody against norepinephrine-synthetic enzyme, tyrosine hydroxylase (TH). Methods. Specimens containing the orbit and the cavernous sinus were obtained from formalin-fixed human cadavers. First, it was confirmed that the superior cervical ganglion

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23

Hu, Xuanming, Mengqian Yuan, Yin Yin, et al. "Electroacupuncture at LI11 promotes jejunal motility via the parasympathetic pathway." BMC Complementary and Alternative Medicine 17, no. 1 (2017): 329. https://doi.org/10.1186/s12906-017-1826-9.

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<strong>Background: </strong>Gastrointestinal motility disorder has been demonstrated to be regulated by acupuncture treatment. The mechanisms underlying the effects of acupuncture stimulation of abdominal and lower limb acupoints on gastrointestinal motility have been thoroughly studied; however, the physiology underlying the effects of acupuncture on the forelimbs to mediate gastrointestinal motility requires further exploration. The aim of this study was to determine whether electroacupuncture (EA) at LI11 promotes jejunal motility, whether the parasympathetic pathway participates in this e

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Putcha, Girish V., Mohanish Deshmukh, and Eugene M. Johnson. "Inhibition of Apoptotic Signaling Cascades Causes Loss of Trophic Factor Dependence during Neuronal Maturation." Journal of Cell Biology 149, no. 5 (2000): 1011–18. http://dx.doi.org/10.1083/jcb.149.5.1011.

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During development, neurons are acutely dependent on target-derived trophic factors for survival. This dependence on trophic support decreases dramatically with maturation in several neuronal populations, including sympathetic neurons. Analyses of nerve growth factor deprivation in immature and mature sympathetic neurons indicate that maturation aborts the cell death pathway at a point that is mechanistically indistinguishable from Bax deletion. However, neither the mRNA nor protein level of BAX changes with neuronal maturation. Therefore, BAX must be regulated posttranslationally in mature ne

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Fernández-González, Juan Francisco, José Ángel García-Pedraza, José Luis Ordóñez, et al. "Renal Sympathetic Hyperactivity in Diabetes Is Modulated by 5-HT1D Receptor Activation via NO Pathway." International Journal of Molecular Sciences 24, no. 2 (2023): 1378. http://dx.doi.org/10.3390/ijms24021378.

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Renal vasculature, which is highly innervated by sympathetic fibers, contributes to cardiovascular homeostasis. This renal sympathetic outflow is inhibited by 5-HT in normoglycaemic rats. Considering that diabetes induces cardiovascular complications, we aimed to determine whether diabetic state modifies noradrenergic input at renal level and its serotonergic modulation in rats. Alloxan diabetic rats were anaesthetized (pentobarbital; 60 mg/kg i.p.) and prepared for in situ autoperfusion of the left kidney to continuously measure systemic blood pressure (SBP), heart rate (HR), and renal perfus

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Al-kuraishy, Hayder M., Ali I. Al-Gareeb, Safaa Qusti, Eida M. Alshammari, Gideon Ampoma Gyebi, and Gaber El-Saber Batiha. "Covid-19-Induced Dysautonomia: A Menace of Sympathetic Storm." ASN Neuro 13 (January 2021): 175909142110576. http://dx.doi.org/10.1177/17590914211057635.

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Among the plethora of debilitating neurological disorders of COVID-19 syndrome in survivors, the scope of SARS-CoV-2-induced dysautonomia (DNS) is yet to be understood, though the implications are enormous. Herein, we present an inclusive mini-review of SARS-CoV-2-induced DNS and its associated complications. Although, the direct link between Covid-19 and DSN is still speculative, the hypothetical links are thought to be either a direct neuronal injury of the autonomic pathway or a para/post-infectious immune-induced mechanism. SARS-CoV-2 infection-induced stress may activate the sympathetic n

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Aboulata, Alaa. "Physiology and immunology of the adrenergic anti-inflammatory pathway." Egyptian journal of Immunology 31, no. 4 (2024): 46–57. http://dx.doi.org/10.55133/eji.310405.

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The adrenergic anti-inflammatory pathway represents a critical intersection between the nervous and immune systems, modulating the body's response to inflammation through the action of catecholamines on adrenergic receptors. This review explored the physiology underlying this pathway, focusing on the mechanisms by which the sympathetic nervous system influences immune function. We delved into the roles of specific adrenergic receptors, primarily the beta-adrenergic receptors, in mediating anti-inflammatory effects, highlighting the involved molecular signaling pathways. Additionally, we examin

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Cechetto, D. F., and S. J. Chen. "Hypothalamic and cortical sympathetic responses relay in the medulla of the rat." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 263, no. 3 (1992): R544—R552. http://dx.doi.org/10.1152/ajpregu.1992.263.3.r544.

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Previously, investigations have indicated that the efferent pathway for sympathetic responses originating in the insular cortex (IC) must initially synapse in the lateral hypothalamic area (LHA). The LHA projects to both the ventrolateral medulla (VLM) and directly to the thoracic spinal cord. To determine the role of the VLM in mediating sympathetic responses from the IC and the LHA, in alpha-chloralose-anesthetized rats, renal nerve responses were recorded following electrical stimulation of these two forebrain sites before and after bilateral injection (300 nl) of cobalt (a synaptic blockin

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Luther, J. A., J. Enes, and S. J. Birren. "Neurotrophins regulate cholinergic synaptic transmission in cultured rat sympathetic neurons through a p75-dependent mechanism." Journal of Neurophysiology 109, no. 2 (2013): 485–96. http://dx.doi.org/10.1152/jn.00076.2011.

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The sympathetic nervous system regulates many essential physiological systems, and its dysfunction is implicated in cardiovascular diseases. Mechanisms that control the strength of sympathetic output are therefore potential targets for the management of these disorders. Here we show that neurotrophins rapidly potentiate cholinergic transmission between cultured rat sympathetic neurons. We found that brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF), acting at the p75 receptor, increased the amplitude of excitatory postsynaptic currents (EPSCs). We observed increased amplit

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30

Simpson, Paul C. "A New Pathway for Sympathetic Cardioprotection in Heart Failure." Circulation Research 117, no. 7 (2015): 592–95. http://dx.doi.org/10.1161/circresaha.115.307246.

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Nase, Geoffrey P., та Matthew A. Boegehold. "Postjunctional α2-adrenoceptors are not present in proximal arterioles of rat intestine". American Journal of Physiology-Heart and Circulatory Physiology 274, № 1 (1998): H202—H208. http://dx.doi.org/10.1152/ajpheart.1998.274.1.h202.

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The purpose of this study was to evaluate two potential stimuli for nitric oxide (NO) release in rat intestinal arterioles during sympathetic nerve activation. To determine whether these vessels contain endothelial α2-adrenoceptors linked to thel-arginine-NO pathway, intravital microscopy was used to study the response of first-order arterioles (1As, 20–40 μm ID) to direct application of 1) the selective α2-agonist BHT-933 and 2) norepinephrine (NE) or sympathetic nerve stimulation before and after α1- or α2-receptor blockade. The effect of sympathetic nerve stimulation on 1A wall shear rate (

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Vaillant, A. R., I. Mazzoni, C. Tudan, M. Boudreau, D. R. Kaplan, and F. D. Miller. "Depolarization and Neurotrophins Converge on the Phosphatidylinositol 3-Kinase–Akt Pathway to Synergistically Regulate Neuronal Survival." Journal of Cell Biology 146, no. 5 (1999): 955–66. http://dx.doi.org/10.1083/jcb.146.5.955.

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In this report, we have examined the mechanisms whereby neurotrophins and neural activity coordinately regulate neuronal survival, focussing on sympathetic neurons, which require target-derived NGF and neural activity for survival during development. When sympathetic neurons were maintained in suboptimal concentrations of NGF, coincident depolarization with concentrations of KCl that on their own had no survival effect, synergistically enhanced survival. Biochemical analysis revealed that depolarization was sufficient to activate a Ras-phosphatidylinositol 3-kinase–Akt pathway (Ras–PI3-kinase–

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Kenney, M. J., and C. K. Ganta. "Autonomic Nervous System and Immune System Interactions." Comprehensive Physiology 4, no. 3 (2014): 1177–200. https://doi.org/10.1002/j.2040-4603.2014.tb00574.x.

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AbstractThe present review assesses the current state of literature defining integrative autonomic‐immune physiological processing, focusing on studies that have employed electrophysiological, pharmacological, molecular biological, and central nervous system experimental approaches. Central autonomic neural networks are informed of peripheral immune status via numerous communicating pathways, including neural and non‐neural. Cytokines and other immune factors affect the level of activity and responsivity of discharges in sympathetic and parasympathetic nerves innervating diverse targets. Multi

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Ren, Xingsheng, Feng Zhang, Mingxia Zhao, et al. "Angiotensin-(1-7) in Paraventricular Nucleus Contributes to the Enhanced Cardiac Sympathetic Afferent Reflex and Sympathetic Activity in Chronic Heart Failure Rats." Cellular Physiology and Biochemistry 42, no. 6 (2017): 2523–39. http://dx.doi.org/10.1159/000480214.

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Background/Aims: Cardiac sympathetic afferent reflex (CSAR) enhancement contributes to exaggerated sympathetic activation in chronic heart failure (CHF). The current study aimed to investigate the roles of angiotensin (Ang)-(1-7) in CSAR modulation and sympathetic activation and Ang-(1-7) signaling pathway in paraventricular nucleus of CHF rats. Methods: CHF was induced by coronary artery ligation. Responses of renal sympathetic nerve activity (RSNA) and mean arterial pressure (MAP) to epicardial application of capsaicin were used to evaluate CSAR in rats with anesthesia. Results: Ang-(1-7) in

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Anggrahini, Dyah Wulan. "Neurohumoral Pathway in Heart Failure." ACI (Acta Cardiologia Indonesiana) 5, no. 1 (P) (2019): 58. http://dx.doi.org/10.22146/aci.47798.

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Heart Failure is now considered as one of the leading cause for mortality and morbidity. It is affecting several organs and cause organ damages due to the myocardial failure to pump inadequate oxygenated blood to the body including metabolites, to end organs and peripheral tissues. Heart failure results from multifactorial mechanism including neurohumoral activations including increased activity of the sympathetic nervous system, renin-angiotensin aldosteron system, vasopression and the atrial natriuretic peptide. This neurohumoral pathway has significant contribution to the development of myo

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Nyhan, D. P., P. W. Clougherty, and P. A. Murray. "AVP-induced pulmonary vasodilation during specific V1 receptor block in conscious dogs." American Journal of Physiology-Heart and Circulatory Physiology 253, no. 3 (1987): H493—H499. http://dx.doi.org/10.1152/ajpheart.1987.253.3.h493.

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Our objectives were 1) to determine whether exogenously administered arginine vasopressin (AVP) can exert a vasoactive influence on the pulmonary circulation of conscious dogs during specific vasopressinergic-1 (V1) receptor block, and 2) to assess the extent to which the pulmonary vascular response to AVP during V1 receptor block is mediated by either sympathetic beta-adrenergic or cholinergic receptor activation or by cyclooxygenase pathway activation. Multipoint pulmonary vascular pressure-cardiac index (P/Q) plots were constructed during normoxia in conscious dogs by stepwise constriction

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Malpas, S. C., and J. H. Coote. "Role of vasopressin in sympathetic response to paraventricular nucleus stimulation in anesthetized rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 266, no. 1 (1994): R228—R236. http://dx.doi.org/10.1152/ajpregu.1994.266.1.r228.

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Vasopressin may play an extrahypothalamic role in the central control of the cardiovascular system, specifically acting as a spinal neurotransmitter in the pathway where the paraventricular nucleus (PVN) alters sympathetic outflow. In this study, the effect of stimulating neuronal cell bodies in the PVN on renal sympathetic nerve activity (RSNA) and the possible involvement of vasopressin in the pathway was investigated in anesthetized rats. The PVN was stimulated by microinjection with 0.2 M D,L-homocysteic acid via a glass micropipette, and the hemodynamic and sympathetic responses were reco

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Li, Sai-Sai, Nan Kang, Xiang-Lei Li, et al. "LianXia Formula Granule Attenuates Cardiac Sympathetic Remodeling in Rats with Myocardial Infarction via the NGF/TrKA/PI3K/AKT Signaling Pathway." Evidence-Based Complementary and Alternative Medicine 2021 (June 11, 2021): 1–11. http://dx.doi.org/10.1155/2021/5536406.

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Sympathetic remodeling may cause severe arrhythmia after myocardial infarction (MI). Thus, targeting this process may be an effective strategy for clinical prevention of arrhythmias. LianXia Formula Granule (LXFG) can effectively improve the symptoms of patients with arrhythmia after MI, and modern pharmacological studies have shown that Coptidis Rhizoma and Rhizoma Pinelliae Preparata, the components of LXFG, have antiarrhythmia effects. Here, we investigated whether LXFG can mitigate sympathetic remodeling and suppress arrhythmia and then elucidated its underlying mechanism of action in rats

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Yang, Peiwei, Xi Chen, Fan Yu, et al. "CAR T cells secreting NGF-neutralizing scFv enhance efficacy in clear cell renal cell carcinoma by relieving immunosuppression through immunosympathectomy." Journal for ImmunoTherapy of Cancer 12, no. 12 (2024): e009910. https://doi.org/10.1136/jitc-2024-009910.

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BackgroundChimeric antigen receptor (CAR) T cells have demonstrated remarkable breakthroughs in treating hematologic malignancies, yet their efficacy in solid tumors is limited by the immunosuppressive microenvironment. Sympathetic nerves significantly contribute to this immunosuppressive milieu in solid tumors. However, the impact of tumor sympathetic denervation on enhancing CAR T-cell antitumor efficacy remains unclear.MethodsWe screened for sympathetic gene sets in various types of cancers and investigated the association of sympathetic nerves with immunosuppression in renal clear cell car

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Zuo, Jinliang. "Functional Pathway Between Cervical Spinal and Sympathetic Ganglia: A Neurochemical Foundation Between Neck Pain and Vertigo." November 2019 6, no. 22;6 (2019): E627—E633. http://dx.doi.org/10.36076/ppj/2019.22.e627.

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Background: Cervical vertigo commonly concurs in patients with neck pain, but the concurrent mechanism of these 2 symptoms still remains unclear. We previously reported a bidirectional segmental nerve fiber connection between cervical spinal and sympathetic ganglia, which provided a hypothesis that this connection between the 2 ganglia may be the anatomic basis for the concurrence of neck pain and cervical vertigo. However, this concurrent mechanism needs biochemical and functional evidence. Objectives: This study aimed to investigate a possible noradrenergic pathway between cervical spinal an

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Amorim-Pires, Diana, Joana Peixoto, and Jorge Lima. "Hypoxia Pathway Mutations in Pheochromocytomas and Paragangliomas." Cytogenetic and Genome Research 150, no. 3-4 (2016): 227–41. http://dx.doi.org/10.1159/000457479.

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Pheochromocytomas (PCC) and sympathetic paragangliomas (PGL) are rare neuroendocrine tumors, which derive from chromaffin cells occurring in the adrenal medulla and extra-adrenal sympathetic paraganglia. PCC and PGL are often benign, catecholamine-producing tumors, responsible for a myriad of symptoms that may be potentially hazardous to the patient. In contrast, nonsecreting parasympathetic PGL, derived from chief cells, develop mainly in the head and neck region. Although PCC/PGL are more commonly sporadic tumors, germline mutations are present in up to 40% of the patients, ranking these tum

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Smith, P. A., and F. F. Weight. "The pathway for the slow inhibitory postsynaptic potential in bullfrog sympathetic ganglia." Journal of Neurophysiology 56, no. 3 (1986): 823–34. http://dx.doi.org/10.1152/jn.1986.56.3.823.

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Intracellular and sucrose gap recording techniques were used to examine synaptically evoked potentials and the response of neurons in bullfrog paravertebral sympathetic ganglia to muscarinic agonists. These neurons were defined as either B or C cells on the basis of the conduction velocity of antidromically evoked action potentials. Following stimulation of preganglionic C-fibers in the rostral portion of the VIIIth spinal nerve, a fast nicotinic excitatory postsynaptic potential (EPSP) and a slow atropine-sensitive inhibitory postsynaptic potential (IPSP) could be recorded intracellularly in

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Rajapakse, Niwanthi W., Beverly Giam, Sanjaya Kuruppu, Geoffrey A. Head, and David M. Kaye. "Impaired l-arginine-nitric oxide pathway contributes to the pathogenesis of resistant hypertension." Clinical Science 133, no. 20 (2019): 2061–67. http://dx.doi.org/10.1042/cs20190851.

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Abstract The precise mechanisms underlying resistant hypertension remain elusive. Reduced nitric oxide (NO) bioavailability is frequently documented in chronic kidney disease, obesity, diabetes and advanced age, all of which are risk factors for resistant hypertension. Sympathetic overactivity and chronic activation of the renin–angiotensin system are salient features of resistant hypertension. Interestingly, recent data indicate that renal sympathetic overactivity can reduce the expression of neuronal nitric oxide synthase in the paraventricular nucleus. Reduced NO levels in the paraventricul

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Leone, Lucia, M. Egle De Stefano, Arianna Del Signore, Tamara C. Petrucci, and Paola Paggi. "Axotomy of Sympathetic Neurons Activates the Metalloproteinase-2 Enzymatic Pathway." Journal of Neuropathology and Experimental Neurology 64, no. 11 (2005): 1007–17. http://dx.doi.org/10.1097/01.jnen.0000187053.59018.3c.

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Gibbins, Ian L., Sue E. Matthew, and Phillip Jobling. "Pathway-specific expression of PKC and PKA in sympathetic neurons." NeuroReport 10, no. 5 (1999): 975–79. http://dx.doi.org/10.1097/00001756-199904060-00015.

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Wang, Putianqi, Ken H. Loh, Michelle Wu, et al. "A leptin–BDNF pathway regulating sympathetic innervation of adipose tissue." Nature 583, no. 7818 (2020): 839–44. http://dx.doi.org/10.1038/s41586-020-2527-y.

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Kunze, D. L., D. Kline, and A. Ramirez-Navarro. "Hypertension in sleep apnea: the role of the sympathetic pathway." Cleveland Clinic Journal of Medicine 74, Suppl_1 (2007): S34. http://dx.doi.org/10.3949/ccjm.74.suppl_1.s34.

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He, Ji-Ye, Xin-Feng Zheng, Sheng-Dan Jiang, Xiao-Dong Chen, and Lei-Sheng Jiang. "Sympathetic neuron can promote osteoblast differentiation through BMP signaling pathway." Cellular Signalling 25, no. 6 (2013): 1372–78. http://dx.doi.org/10.1016/j.cellsig.2013.02.016.

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Saleemi, Saadat Ali, and Ramesh Sahathevan. "Horner’s syndrome secondary to internal carotid artery occlusion." BMJ Case Reports 14, no. 2 (2021): e234973. http://dx.doi.org/10.1136/bcr-2020-234973.

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Horner’s syndrome results from interruption of the sympathetic innervation to the eye. This interruption may occur at three anatomical levels along the sympathetic trunk pathway. There are numerous causes of Horner’s syndrome, including injury to the carotid artery, of which arterial dissection is the commonest pathology. Occlusive carotid disease secondary to atherosclerosis is a relatively rare cause of Horner’s syndrome. We describe a patient with Horner’s syndrome due to complete occlusion of the ipsilateral internal carotid artery.

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Min, Sun Ki, Jinyoung Oh, Taemin Kim, Ji Eun Han, Sang Won Han, and Hyun-jeung Yu. "Laterality of Skin Temperature and Magnetic Resonance Imaging in Patients with Wallenberg Syndrome." Journal of Neurosonology and Neuroimaging 13, no. 2 (2021): 47–54. http://dx.doi.org/10.31728/jnn.2021.00101.

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Background: Recently, lateral differences in body surface temperature (BST) have been reported as a symptom of Wallenberg syndrome (WS), resulting from disturbances in the sympathetic nerve pathway. This study aimed to investigate the relationship between the laterality of BST and brain magnetic resonance imaging (MRI) findings in 12 patients with WS.Methods: BST was measured using an infrared thermal camera at 7±3 days and 90±30 days after symptom onset. The MRI findings were categorized as rostral, middle, and caudal medulla rostrocaudally and typical, ventral, large, dorsal, and lateral typ

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