INT61591

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Context Info
Confidence 0.59
First Reported 1995
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 11
Total Number 11
Disease Relevance 2.09
Pain Relevance 0.85

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 4
blood 2
EDN1 (Homo sapiens)
Pain Link Frequency Relevance Heat
Opioid 1 99.64 Very High Very High Very High
antagonist 17 98.72 Very High Very High Very High
Angina 3 97.92 Very High Very High Very High
bradykinin 1 97.16 Very High Very High Very High
ischemia 3 97.00 Very High Very High Very High
Inflammation 3 97.00 Very High Very High Very High
Neuropeptide 2 93.60 High High
metalloproteinase 4 90.96 High High
Endogenous opioid 2 89.72 High High
Potency 1 82.88 Quite High
Disease Link Frequency Relevance Heat
Natriuresis 1 99.30 Very High Very High Very High
Atherosclerosis 3 98.72 Very High Very High Very High
Cv General 3 Under Development 3 97.92 Very High Very High Very High
Coronary Artery Disease 12 97.44 Very High Very High Very High
Hypotension 8 97.36 Very High Very High Very High
INFLAMMATION 3 97.00 Very High Very High Very High
Hypoxia 2 95.44 Very High Very High Very High
Stress 8 95.08 Very High Very High Very High
Hypertension 69 93.48 High High
Syndrome 5 87.12 High 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.
Negative_regulation (block) of Localization (released) of ET-1 associated with angina, coronary artery disease, atherosclerosis, ischemia and antagonist
1) Confidence 0.59 Published 1995 Journal J. Cardiovasc. Pharmacol. Section Abstract Doc Link 8587420 Disease Relevance 0.29 Pain Relevance 0.23
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).
Negative_regulation (reduction) of Localization (release) of ET-1
2) Confidence 0.57 Published 2008 Journal Vascular Health and Risk Management Section Body Doc Link PMC2515431 Disease Relevance 0.09 Pain Relevance 0
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.
Negative_regulation (effect) of Localization (release) of ET-1
3) Confidence 0.57 Published 2009 Journal Anesthesiology Section Body Doc Link 19104173 Disease Relevance 0 Pain Relevance 0
Figure 2b shows that the ET-1-induced NO release was significantly inhibited by p38 inhibition and prevented by KT5720, a PKA inhibitor.
Negative_regulation (prevented) of Localization (release) of ET-1-induced
4) Confidence 0.52 Published 2005 Journal Arthritis Res Ther Section Body Doc Link PMC1065327 Disease Relevance 0 Pain Relevance 0
In addition, POMC gene delivery significantly decreased the ET-1 release (P < 0.001) without affecting the ET-1 messenger RNA (mRNA) level.
Negative_regulation (decreased) of Localization (release) of ET-1
5) Confidence 0.48 Published 2006 Journal Exp. Biol. Med. (Maywood) Section Abstract Doc Link 16740999 Disease Relevance 0.21 Pain Relevance 0.14
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.
Negative_regulation (inhibits) of Localization (secretion) of ET-1 in endothelial cells
6) Confidence 0.42 Published 2009 Journal Anesthesiology Section Body Doc Link 19104173 Disease Relevance 0 Pain Relevance 0
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.
Negative_regulation (reversed) of Localization (release) of ET-1
7) Confidence 0.42 Published 2009 Journal Anesthesiology Section Body Doc Link 19104173 Disease Relevance 0 Pain Relevance 0
Figure 2b shows that the ET-1-induced NO release was significantly inhibited by p38 inhibition and prevented by KT5720, a PKA inhibitor.
Negative_regulation (inhibited) of Localization (release) of ET-1-induced
8) Confidence 0.38 Published 2005 Journal Arthritis Res Ther Section Body Doc Link PMC1065327 Disease Relevance 0 Pain Relevance 0
Blockade of endothelin-1 release contributes to the anti-angiogenic effect by pro-opiomelanocortin overexpression in endothelial cells.
Negative_regulation (Blockade) of Localization (release) of endothelin-1 in endothelial cells
9) Confidence 0.35 Published 2006 Journal Exp. Biol. Med. (Maywood) Section Title Doc Link 16740999 Disease Relevance 0.25 Pain Relevance 0.14
Alternative mechanisms, such as such as opioid-like activities, inhibition of the release of the vasoactive substances such as the vasoconstrictor endothelin-1, eicosanoids and nitric oxide have been proposed to underlie the blood pressure lowering effect of lactotripeptides (see [38] for a review).
Negative_regulation (inhibition) of Localization (release) of endothelin-1 in blood associated with hypotension and opioid
10) Confidence 0.10 Published 2010 Journal Nutr J Section Body Doc Link PMC2989300 Disease Relevance 0.50 Pain Relevance 0.19
In contrast, nitric oxide, natriuretic peptides, and dilator prostanoids inhibit endothelin release.
Negative_regulation (inhibit) of Localization (release) of endothelin associated with natriuresis
11) Confidence 0.05 Published 2010 Journal Vascular Health and Risk Management Section Body Doc Link PMC3004515 Disease Relevance 0.75 Pain Relevance 0.16

General Comments

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