"Sympatholytics" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus,
MeSH (Medical Subject Headings). Descriptors are arranged in a hierarchical structure,
which enables searching at various levels of specificity.
Drugs that inhibit the actions of the sympathetic nervous system by any mechanism. The most common of these are the ADRENERGIC ANTAGONISTS and drugs that deplete norepinephrine or reduce the release of transmitters from adrenergic postganglionic terminals (see ADRENERGIC AGENTS). Drugs that act in the central nervous system to reduce sympathetic activity (e.g., centrally acting alpha-2 adrenergic agonists, see ADRENERGIC ALPHA-AGONISTS) are included here.
| Descriptor ID |
D013565
|
| MeSH Number(s) |
D27.505.696.663.050.850
|
| Concept/Terms |
Sympatholytics- Sympatholytics
- Sympatholytic Agents
- Agents, Sympatholytic
- Sympatholytic Drugs
- Drugs, Sympatholytic
- Sympathetic-Blocking Agents
- Agents, Sympathetic-Blocking
- Sympathetic Blocking Agents
Sympatholytic Effect- Sympatholytic Effect
- Effect, Sympatholytic
- Sympatholytic Effects
- Effects, Sympatholytic
|
Below are MeSH descriptors whose meaning is more general than "Sympatholytics".
Below are MeSH descriptors whose meaning is more specific than "Sympatholytics".
This graph shows the total number of publications written about "Sympatholytics" by people in this website by year, and whether "Sympatholytics" was a major or minor topic of these publications.
To see the data from this visualization as text,
click here.
| Year | Major Topic | Minor Topic | Total |
|---|
| 1994 | 0 | 1 | 1 |
| 1996 | 1 | 1 | 2 |
| 1999 | 0 | 1 | 1 |
| 2004 | 0 | 1 | 1 |
| 2005 | 0 | 1 | 1 |
| 2007 | 0 | 1 | 1 |
| 2008 | 0 | 2 | 2 |
| 2010 | 0 | 1 | 1 |
| 2011 | 0 | 1 | 1 |
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Below are the most recent publications written about "Sympatholytics" by people in Profiles.
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Transfer of host-derived a synuclein to grafted dopaminergic neurons in rat. Neurobiol Dis. 2011 Sep; 43(3):552-7.
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Evidence-based interventional pain medicine according to clinical diagnoses. 16. Complex regional pain syndrome. Pain Pract. 2011 Jan-Feb; 11(1):70-87.
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Future of cell and gene therapies for Parkinson's disease. Ann Neurol. 2008 Dec; 64 Suppl 2:S122-38.
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Fos expression following activation of the ventral pallidum in normal rats and in a model of Parkinson's Disease: implications for limbic system and basal ganglia interactions. Brain Struct Funct. 2008 Sep; 213(1-2):197-213.
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AAV2-mediated delivery of human neurturin to the rat nigrostriatal system: long-term efficacy and tolerability of CERE-120 for Parkinson's disease. Neurobiol Dis. 2007 Jul; 27(1):67-76.
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Focal not widespread grafts induce novel dyskinetic behavior in parkinsonian rats. Neurobiol Dis. 2006 Jan; 21(1):165-80.
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Limbic pallidal adaptations following long-term cessation of dopaminergic transmission: lack of upregulation of dopamine receptor function. Exp Neurol. 2004 Apr; 186(2):145-57.
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Caspase-3-like proteases and 6-hydroxydopamine induced neuronal cell death. Brain Res Mol Brain Res. 1999 Jan 22; 64(1):141-8.
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Loss of striatal DA innervation increases striatal trophic activity directed at DA neurons in culture. Exp Neurol. 1996 Aug; 140(2):184-97.
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Intrathecal clonidine and tizanidine in conscious dogs: comparison of analgesic and hemodynamic effects. Anesth Analg. 1996 Mar; 82(3):627-35.