INT9191

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Context Info
Confidence 0.81
First Reported 1992
Last Reported 2011
Negated 0
Speculated 0
Reported most in Abstract
Documents 94
Total Number 95
Disease Relevance 57.01
Pain Relevance 14.78

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
endothelial cells 13
smooth muscle 4
epithelial cells 4
macrophage 3
vascular endothelium 3
EDN1 (Homo sapiens)
Pain Link Frequency Relevance Heat
Inflammation 490 100.00 Very High Very High Very High
Inflammatory mediators 22 100.00 Very High Very High Very High
qutenza 19 100.00 Very High Very High Very High
antagonist 874 99.92 Very High Very High Very High
Serotonin 44 99.80 Very High Very High Very High
Neuropeptide 16 99.42 Very High Very High Very High
Opioid 9 99.28 Very High Very High Very High
Somatostatin 8 99.00 Very High Very High Very High
Pain 98 98.96 Very High Very High Very High
Dismenorea 3 98.72 Very High Very High Very High
Disease Link Frequency Relevance Heat
INFLAMMATION 557 100.00 Very High Very High Very High
Cancer 266 100.00 Very High Very High Very High
Diabetic Nephropathy 18 99.96 Very High Very High Very High
Sprains And Strains 30 99.58 Very High Very High Very High
Reprotox - General 1 78 99.52 Very High Very High Very High
Increased Venous Pressure Under Development 997 99.46 Very High Very High Very High
Pulmonary Hypertension 1824 99.32 Very High Very High Very High
Diabetes Mellitus 868 99.20 Very High Very High Very High
Papillomavirus Infection 12 99.16 Very High Very High Very High
Natriuresis 52 99.14 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Bosentan is an orally active ET-1 antagonist, and these results suggest that this compound might be used to block the effects of locally released ET-1 in pathologic conditions, such as atherosclerosis, angina, and myocardial ischemia.
Localization (released) of ET-1 associated with angina, coronary artery disease, atherosclerosis, ischemia and antagonist
1) Confidence 0.81 Published 1995 Journal J. Cardiovasc. Pharmacol. Section Abstract Doc Link 8587420 Disease Relevance 0.29 Pain Relevance 0.23
Using cultured human aortic endothelial cells, we examined the effects of phosphoramidon, an endothelin converting enzyme (ECE) inhibitor, on the release of endogenous endothelin-1 (ET-1) and big endothelin-1 (big ET-1), and on the generation of ET-1 from exogenously applied big ET-1.
Localization (release) of endothelin-1 in endothelial cells
2) Confidence 0.80 Published 1995 Journal Biol. Pharm. Bull. Section Abstract Doc Link 7550091 Disease Relevance 0 Pain Relevance 0
When high concentrations of phosphoramidon were added, there was a dramatic increase in the release of big ET-1, which cannot be explained only by the drug-induced inhibition of ECE.
Localization (release) of ET-1
3) Confidence 0.80 Published 1995 Journal Biol. Pharm. Bull. Section Abstract Doc Link 7550091 Disease Relevance 0 Pain Relevance 0
Phosphoramidon, at concentrations of 10(-6) to 2 x 10(-4) M, caused a biphasic alteration of the ET-1 release, i.e., at lower concentrations of the drug, there were slight but unexpected increases of the release, whereas higher concentrations led to a decrease which is due to the drug-induced inhibition of ECE.
Localization (release) of ET-1
4) Confidence 0.80 Published 1995 Journal Biol. Pharm. Bull. Section Abstract Doc Link 7550091 Disease Relevance 0 Pain Relevance 0
Phosphoramidon enhanced the big ET-1 release from the cells in a concentration-dependent manner.
Localization (release) of ET-1
5) Confidence 0.80 Published 1995 Journal Biol. Pharm. Bull. Section Abstract Doc Link 7550091 Disease Relevance 0 Pain Relevance 0
This increase in big ET-1 release appeared to be partly due to a transient stimulation of the expression of prepro ET-1 mRNA.
Localization (release) of ET-1
6) Confidence 0.80 Published 1995 Journal Biol. Pharm. Bull. Section Abstract Doc Link 7550091 Disease Relevance 0 Pain Relevance 0
The former effect appears to be based on the inhibition of ET-1 degradation by neutral endopeptidase 24.11 (NEP), since kelatorphan, a specific NEP inhibitor, produced a similar increasing effect on ET-1 release.
Localization (release) of ET-1
7) Confidence 0.80 Published 1995 Journal Biol. Pharm. Bull. Section Abstract Doc Link 7550091 Disease Relevance 0 Pain Relevance 0
Using cultured human aortic endothelial cells, we examined the effects of phosphoramidon, an endothelin converting enzyme (ECE) inhibitor, on the release of endogenous endothelin-1 (ET-1) and big endothelin-1 (big ET-1), and on the generation of ET-1 from exogenously applied big ET-1.
Localization (release) of endothelin-1 in endothelial cells
8) Confidence 0.80 Published 1995 Journal Biol. Pharm. Bull. Section Abstract Doc Link 7550091 Disease Relevance 0 Pain Relevance 0
Using cultured human aortic endothelial cells, we examined the effects of phosphoramidon, an endothelin converting enzyme (ECE) inhibitor, on the release of endogenous endothelin-1 (ET-1) and big endothelin-1 (big ET-1), and on the generation of ET-1 from exogenously applied big ET-1.
Localization (release) of ET-1 in endothelial cells
9) Confidence 0.80 Published 1995 Journal Biol. Pharm. Bull. Section Abstract Doc Link 7550091 Disease Relevance 0 Pain Relevance 0
Using cultured human aortic endothelial cells, we examined the effects of phosphoramidon, an endothelin converting enzyme (ECE) inhibitor, on the release of endogenous endothelin-1 (ET-1) and big endothelin-1 (big ET-1), and on the generation of ET-1 from exogenously applied big ET-1.
Localization (release) of ET-1 in endothelial cells
10) Confidence 0.80 Published 1995 Journal Biol. Pharm. Bull. Section Abstract Doc Link 7550091 Disease Relevance 0 Pain Relevance 0
The above vasoactive coronary properties of estrogen may be mediated via promotion of the release or action of potentially beneficial substances, such as nitric oxide (Gueta et al 1997; Rosano et al 1997; Best et al 1998) or via reduction of the release or action of potentially adverse mediators such as ET-1 (Jiang et al 1992; Lerman et al 1995; Lamping et al 1996; Sudhir et al 1996, 1997; Webb et al 2000).
Localization (release) of ET-1
11) Confidence 0.79 Published 2008 Journal Vascular Health and Risk Management Section Body Doc Link PMC2515431 Disease Relevance 0.09 Pain Relevance 0
CONCLUSIONS: The authors demonstrate for the first time that propofol inhibits strain-induced ET-1 secretion and enhances strain-increased nitric oxide production in human umbilical vein endothelial cells.
Localization (secretion) of ET-1 in endothelial cells
12) Confidence 0.78 Published 2009 Journal Anesthesiology Section Body Doc Link 19104173 Disease Relevance 0 Pain Relevance 0
The aims of this study were to test the hypothesis that propofol may alter strain-induced endothelin-1 (ET-1) secretion and nitric oxide production, and to identify the putative underlying signaling pathways in human umbilical vein endothelial cells.
Localization (secretion) of endothelin-1 in endothelial cells associated with sprains and strains
13) Confidence 0.78 Published 2009 Journal Anesthesiology Section Abstract Doc Link 19104173 Disease Relevance 0.27 Pain Relevance 0.09
Furthermore, in the presence of PTIO, a nitric oxide scavenger, and KT5823, a specific inhibitor of cyclic guanosine monophosphate-dependent protein kinase, the inhibitory effect of propofol on strain-induced extracellular signal-regulated protein kinase phosphorylation and ET-1 release was reversed.
Localization (release) of ET-1
14) Confidence 0.78 Published 2009 Journal Anesthesiology Section Body Doc Link 19104173 Disease Relevance 0 Pain Relevance 0
The aims of this study were to test the hypothesis that propofol may alter strain-induced endothelin-1 (ET-1) secretion and nitric oxide production, and to identify the putative underlying signaling pathways in human umbilical vein endothelial cells.
Localization (secretion) of ET-1 in endothelial cells associated with sprains and strains
15) Confidence 0.78 Published 2009 Journal Anesthesiology Section Abstract Doc Link 19104173 Disease Relevance 0.27 Pain Relevance 0.09
In vitro, oxyhemoglobin stimulates the secretion of endothelin (ET)-1, a vasoconstrictor, inhibits the vasodilator nitric oxide (NO) and produces activated oxygen species [23-25].
Localization (secretion) of endothelin
16) Confidence 0.78 Published 2007 Journal Crit Care Section Body Doc Link PMC2206512 Disease Relevance 1.01 Pain Relevance 0.25
ET-1 is secreted by glomerular endothelial cells, mesangial cells, and epithelial cells.
Localization (secreted) of ET-1 in epithelial cells
17) Confidence 0.76 Published 2008 Journal Vascular Health and Risk Management Section Body Doc Link PMC2605330 Disease Relevance 0.74 Pain Relevance 0
As tumor expression and release of ET-1 has been shown to be regulated by the local environment, location specific expression and release of ET-1 by tumor cells may provide insight into the mechanisms that underlie the heterogeneity of bone cancer pain that is frequently observed in humans with multiple skeletal metastases.
Localization (release) of ET-1 associated with cancer pain, cancer and metastasis
18) Confidence 0.76 Published 2004 Journal Neuroscience Section Abstract Doc Link 15207337 Disease Relevance 1.09 Pain Relevance 0.65
We report that myometrial cells under basal conditions not only respond to but also secrete ET-1, one of the main regulators of uterine contractions.
Localization (secrete) of ET-1 in uterine associated with dismenorea
19) Confidence 0.75 Published 2005 Journal Endocrinology Section Abstract Doc Link 16109787 Disease Relevance 0.17 Pain Relevance 0.18
Figure 2a shows that ET-1 greatly stimulated NO production and was released in a concentration-dependent manner.
Localization (released) of ET-1
20) Confidence 0.72 Published 2005 Journal Arthritis Res Ther Section Body Doc Link PMC1065327 Disease Relevance 0 Pain Relevance 0

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