INT24768

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Context Info
Confidence 0.43
First Reported 1989
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 10
Total Number 10
Disease Relevance 2.85
Pain Relevance 1.48

This is a graph with borders and nodes. Maybe there is an Imagemap used so the nodes may be linking to some Pages.

extracellular space (Edn1) extracellular region (Edn1) cell-cell signaling (Edn1)
cytoplasm (Edn1)
Anatomy Link Frequency
ventral root 2
endothelial cells 2
smooth muscle cells 2
musculoskeletal system 2
vascular endothelium 2
Edn1 (Rattus norvegicus)
Pain Link Frequency Relevance Heat
antagonist 54 99.96 Very High Very High Very High
Spinal cord 7 98.64 Very High Very High Very High
substance P 4 97.28 Very High Very High Very High
qutenza 54 97.08 Very High Very High Very High
agonist 28 93.20 High High
Intracerebroventricular 1 87.64 High High
Central nervous system 1 85.84 High High
alcohol 3 83.12 Quite High
Sciatic nerve 1 82.16 Quite High
Neurotransmitter 5 81.92 Quite High
Disease Link Frequency Relevance Heat
Increased Venous Pressure Under Development 9 99.16 Very High Very High Very High
Hypertension 37 98.12 Very High Very High Very High
Hiatal Hernia 111 96.52 Very High Very High Very High
Stroke 1 93.76 High High
Pressure Volume 2 Under Development 6 92.64 High High
Atherosclerosis 4 82.60 Quite High
Myocardial Infarction 2 76.92 Quite High
Sudden Death 1 76.16 Quite High
Cv General 3 Under Development 1 75.60 Quite High
Cardiovascular Disease 3 75.12 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Bath-applied ET-1 produced a depolarization of a lumbar ventral root, which was suppressed by nicardipine or a substance P antagonist (spantide).
Negative_regulation (depolarization) of Gene_expression (produced) of ET-1 in ventral root associated with antagonist and substance p
1) Confidence 0.43 Published 1989 Journal J. Cardiovasc. Pharmacol. Section Abstract Doc Link 2473317 Disease Relevance 0 Pain Relevance 0.32
ET-1 produced a reduction in blood flow to the brain (83%), heart (62%), kidneys (53%), gastrointestinal tract (43%), portal system (46%), and musculoskeletal system (55%).
Negative_regulation (reduction) of Gene_expression (produced) of ET-1 in musculoskeletal system
2) Confidence 0.43 Published 1997 Journal Am. J. Physiol. Section Abstract Doc Link 9321804 Disease Relevance 0.34 Pain Relevance 0.12
NO reduces ET-1 synthesis[25] and counteracts vasoconstriction initiated by ETA-receptors on smooth muscle cells[4], [7], [26].
Negative_regulation (reduces) of Gene_expression (synthesis) of ET-1 in smooth muscle cells associated with increased venous pressure under development
3) Confidence 0.43 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2879375 Disease Relevance 0.22 Pain Relevance 0.15
Inhibitors of endothelin (ET), which is a potent vasoconstrictor produced in the vascular endothelium, may also improve pulmonary hypertension.
Negative_regulation (Inhibitors) of Gene_expression (produced) of endothelin in vascular endothelium associated with hypertension
4) Confidence 0.41 Published 2009 Journal Pediatr Surg Int Section Body Doc Link PMC2734260 Disease Relevance 1.08 Pain Relevance 0.07
Conversely, nitric oxide can inhibit ET-1 synthesis in different cell types (Takada et al. 1996).
Negative_regulation (inhibit) of Gene_expression (synthesis) of ET-1
5) Confidence 0.39 Published 2008 Journal Gene Regulation and Systems Biology Section Body Doc Link PMC2733097 Disease Relevance 0 Pain Relevance 0
The production of nitric oxide is activated by ET-1 while the elevated nitric oxide level is able to inhibit ET-1 synthesis (Namiki et al. 1992; Takada et al. 1996).
Negative_regulation (inhibit) of Gene_expression (synthesis) of ET-1
6) Confidence 0.39 Published 2008 Journal Gene Regulation and Systems Biology Section Body Doc Link PMC2733097 Disease Relevance 0 Pain Relevance 0.03
Potentiation was completely prevented by a 2 minute incubation with BIM X (500 nM) prior to the ET-1 application (Fig. 6A).
Negative_regulation (prevented) of Gene_expression (application) of ET-1
7) Confidence 0.39 Published 2007 Journal Mol Pain Section Body Doc Link PMC2206006 Disease Relevance 0 Pain Relevance 0.35
BQ-123 (cyclo(D-Trp,D-Asp,L-Pro,D-Val,L-Leu), a selective endothelin ETA receptor antagonist, reduced the endothelin-1- and endothelin-3-induced [3H]inositol phosphate production, with similar inhibition constants (IC50: 16.7 +/- 3.4 and 8.0 +/- 1.6 microM, respectively).
Negative_regulation (reduced) of Gene_expression (production) of endothelin-1 associated with antagonist
8) Confidence 0.37 Published 1996 Journal Eur. J. Pharmacol. Section Abstract Doc Link 8982672 Disease Relevance 0 Pain Relevance 0.21
CONCLUSIONS: The results suggest that suppression of ET-1 generation counters the mucosal drop in cNOS and the extent of gastric mucosal damage caused by indomethacin, but has no effect on the mucosal responses associated with up-regulation of NOS-2 expression.
Negative_regulation (suppression) of Gene_expression (generation) of ET-1
9) Confidence 0.37 Published 2000 Journal Scand. J. Gastroenterol. Section Body Doc Link 11145282 Disease Relevance 0.05 Pain Relevance 0
The mechanisms include antiplatelet actions, increases in high-density lipoprotein, antioxidation, reduced endothelin-1 production, and increased endothelial nitric oxide synthase expression which causes augmented nitric oxide production by endothelial cells.
Negative_regulation (reduced) of Gene_expression (production) of endothelin-1 in endothelial cells
10) Confidence 0.18 Published 2004 Journal Braz. J. Med. Biol. Res. Section Abstract Doc Link 15334193 Disease Relevance 1.15 Pain Relevance 0.23

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