INT54886

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Context Info
Confidence 0.42
First Reported 1993
Last Reported 2011
Negated 1
Speculated 0
Reported most in Body
Documents 25
Total Number 25
Disease Relevance 9.33
Pain Relevance 3.79

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

cell differentiation (ANGPT2) signal transduction (ANGPT2) extracellular space (ANGPT2)
extracellular region (ANGPT2) plasma membrane (ANGPT2) nucleus (ANGPT2)
Anatomy Link Frequency
plasma 2
blood 1
neuronal 1
endothelial cell 1
aorta 1
ANGPT2 (Homo sapiens)
Pain Link Frequency Relevance Heat
Bioavailability 3 98.96 Very High Very High Very High
antagonist 39 98.24 Very High Very High Very High
Angina 25 97.92 Very High Very High Very High
bradykinin 28 94.84 High High
midbrain 4 93.32 High High
cva 7 84.12 Quite High
headache 5 76.96 Quite High
backache 5 76.16 Quite High
Central nervous system 9 76.12 Quite High
Inflammation 13 75.00 Quite High
Disease Link Frequency Relevance Heat
Hypertension 47 99.12 Very High Very High Very High
Cv General 3 Under Development 29 97.92 Very High Very High Very High
Natriuresis 17 97.00 Very High Very High Very High
Cv Unclassified Under Development 25 96.24 Very High Very High Very High
Myocardial Infarction 148 93.00 High High
Apoptosis 8 91.96 High High
Headache 26 91.60 High High
Coronary Heart Disease 8 89.52 High High
Cardiovascular Disease 24 89.28 High High
Pathologic Constriction 11 88.60 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Its contractile inhibition was not affected by Ang II antiserum and diminished the Ang II contraction at high micromolar concentrations, findings consistent with physicochemical data showing that it is an Ang II complement.
Neg (not) Negative_regulation (diminished) of Ang II
1) Confidence 0.42 Published 1998 Journal Hypertension Section Abstract Doc Link 9495272 Disease Relevance 0 Pain Relevance 0.11
The facilitatory effect of Ang II was blocked by either the peptide Ang II receptor antagonist saralasin (1.0 mumol/L) or EXP 3174 (0.1 mumol/L), the in vitro active form of the nonpeptide Ang II receptor antagonist losartan.
Negative_regulation (effect) of Ang II associated with antagonist
2) Confidence 0.31 Published 1994 Journal Circ. Res. Section Abstract Doc Link 8118951 Disease Relevance 0 Pain Relevance 0.26
A combination treatment that includes Dll4, Ang2, and a Jak kinase inhibitor, previously shown to increase NSC expansion in vivo [31] (Combination Treatment, “CT”) supports cell growth from the lateral regions of the forebrain and the ventral midbrain (Figure 1B, C, F).
Negative_regulation (inhibitor) of Ang2 in forebrain associated with midbrain
3) Confidence 0.25 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2829079 Disease Relevance 0 Pain Relevance 0.12
The VEGF and Ang-2 protein levels in supernatants of the culture medium were decreased gradually in a concentration-dependent or time-dependent fashion.
Negative_regulation (decreased) of Ang-2 protein
4) Confidence 0.20 Published 2007 Journal J. Huazhong Univ. Sci. Technol. Med. Sci. Section Abstract Doc Link 17828495 Disease Relevance 0.07 Pain Relevance 0.06
Our findings may indirectly support a positive effect of ACE/Ang II inhibition on the frequency and severity of migraine attacks, as observed in other studies and reports.


Negative_regulation (inhibition) of Ang II
5) Confidence 0.12 Published 2004 Journal Pharmacoepidemiol Drug Saf Section Body Doc Link 14971122 Disease Relevance 0 Pain Relevance 0
In contrast to these antiproliferative and antimigratory effects, an enhancement of endothelial cell migration has been demonstrated with ACE-I with reduced Ang II that may contribute to improved endothelial function and might therefore exert an antiatherosclerotic action.


Negative_regulation (reduced) of Ang II in endothelial cell
6) Confidence 0.11 Published 2008 Journal Vascular Health and Risk Management Section Body Doc Link PMC2663435 Disease Relevance 0.57 Pain Relevance 0.16
Aliskiren produced dose-dependent reductions in PRA, Ang I, and Ang II vs placebo.
Negative_regulation (reductions) of Ang II
7) Confidence 0.10 Published 2010 Journal Vascular Health and Risk Management Section Body Doc Link PMC2922316 Disease Relevance 1.01 Pain Relevance 0.13
The TI fluctuation estimate, after relative to 'during', had increased by 50.3% after ACE/Ang II inhibition and had reduced by 22.2% after diuretic treatment (p = 0.1).
Negative_regulation (inhibition) of Ang II
8) Confidence 0.08 Published 2004 Journal Pharmacoepidemiol Drug Saf Section Body Doc Link 14971122 Disease Relevance 0 Pain Relevance 0
For patients who continued abortive migraine drug use during and after ACE/Ang II or diuretic therapy, a significantly larger reduction in this estimate was observed during ACE/Ang II inhibition (68.9%) compared to during diuretic therapy (10.5% increase) (p = 0.004).
Negative_regulation (inhibition) of Ang II
9) Confidence 0.08 Published 2004 Journal Pharmacoepidemiol Drug Saf Section Body Doc Link 14971122 Disease Relevance 0.10 Pain Relevance 0
The effects of ACE/Ang II inhibition as well as diuretic therapy on reducing the frequency of migraine attacks were assessed by measuring the mean consumption of abortive migraine drug use, in DDDs per month ('therapeutic intensity'), before, during and after ACE/Ang II or diuretic therapy.
Negative_regulation (inhibition) of Ang II
10) Confidence 0.08 Published 2004 Journal Pharmacoepidemiol Drug Saf Section Body Doc Link 14971122 Disease Relevance 0.17 Pain Relevance 0
Vascular and cardioprotective properties of ACE-I largely result from their effects in inhibiting Ang II formation.
Negative_regulation (inhibiting) of Ang II
11) Confidence 0.08 Published 2008 Journal Vascular Health and Risk Management Section Body Doc Link PMC2663435 Disease Relevance 0.38 Pain Relevance 0.13
Similarly, Ang II decreased and remained below placebo for 48 hours (P < 0.05).
Negative_regulation (decreased) of Ang II
12) Confidence 0.07 Published 2010 Journal Vascular Health and Risk Management Section Body Doc Link PMC2922316 Disease Relevance 0.07 Pain Relevance 0
Again, aliskiren at a dose of 300 mg decreases PRA in hypertensive patients by approximately 50%–80%51,52 and reduces PRA and plasma levels of Ang I and Ang II for 48 hours.53 Furthermore, urinary aldosterone was reduced at a dose of 80 mg or more, and sodium extraction was increased to 91% at a dose of 640 mg.54 Compared with valsartan, aliskiren more strongly decreases the activity of renin in the circulation and reduces the excretion of urinary aldosterone for a longer period.53,55 Following oral administration, peak plasma concentrations of aliskiren are reached within 1–3 hours.52,53,56–58 The plasma half-life of aliskiren in humans shows a slow terminal elimination at 23–70 hours59–61 and approximately 47%–51% of aliskiren is bound by plasma proteins in humans, independent of the concentration.59,62,63 Based on in vitro studies, the major enzyme responsible for its metabolism appears to be Cytochrome P450 (CYP3A4).
Negative_regulation (reduces) of Ang II in plasma associated with hypertension
13) Confidence 0.07 Published 2010 Journal Vascular Health and Risk Management Section Body Doc Link PMC2922316 Disease Relevance 0.10 Pain Relevance 0
In healthy humans, aliskiren of doses between 40 and 640 mg exerts a dose-dependent reduction in PRA, Ang I, and Ang II levels.
Negative_regulation (reduction) of Ang II
14) Confidence 0.07 Published 2010 Journal Vascular Health and Risk Management Section Body Doc Link PMC2922316 Disease Relevance 0.09 Pain Relevance 0
In healthy human subjects, doses of between 40 and 640 mg of aliskiren exert a dose-dependent reduction in PRA and Ang I and Ang II levels.
Negative_regulation (reduction) of Ang II
15) Confidence 0.07 Published 2008 Journal Pharmacol Rep Section Abstract Doc Link 19066408 Disease Relevance 0.39 Pain Relevance 0.20
Although both surgical methods had similar effects on Ang 1, Ang 2, and the Ang 1/Ang 2 ratio, the extent of the changes (decrease in Ang 1, increase in Ang 2, and decrease in the Ang 1/ Ang 2 ratio) was significantly greater after open colorectal resection.
Negative_regulation (decrease) of Ang 2
16) Confidence 0.06 Published 2009 Journal Surg Endosc Section Body Doc Link PMC2814196 Disease Relevance 0.14 Pain Relevance 0
METHODS: Data from a large prescription database involving 95 patients initiating a specific abortive migraine drug (ergotamine or a triptan) and subsequently treated with either an ACE inhibitor or angiotensin receptor antagonist (index group: ACE/Ang II) or diuretic (reference group) were analysed.
Negative_regulation (inhibitor) of Ang II
17) Confidence 0.04 Published 2004 Journal Pharmacoepidemiol Drug Saf Section Body Doc Link 14971122 Disease Relevance 0.18 Pain Relevance 0
Ang II blockade at the receptor level may thus be more efficient than ACE inhibition in blocking the undesirable cardiovascular actions of Ang II.
Negative_regulation (blockade) of Ang II
18) Confidence 0.04 Published 1993 Journal J Hypertens Suppl Section Abstract Doc Link 8315523 Disease Relevance 0.35 Pain Relevance 0.17
POTENTIAL OF ANGIOTENSIN (ANG) II ANTAGONISTS: Ang II antagonists are expected to produce similar beneficial effects to those of ACE inhibitors, through blockade of vascular, adrenal, renal and prejunctional neuronal Ang II type 1 receptors.
Negative_regulation (blockade) of Ang II in neuronal associated with antagonist
19) Confidence 0.03 Published 1993 Journal J Hypertens Suppl Section Abstract Doc Link 8315523 Disease Relevance 0.49 Pain Relevance 0.21
Ang II blockade at the receptor level may thus be more efficient than ACE inhibition in blocking the undesirable cardiovascular actions of Ang II.
Negative_regulation (blocking) of Ang II
20) Confidence 0.03 Published 1993 Journal J Hypertens Suppl Section Abstract Doc Link 8315523 Disease Relevance 0.34 Pain Relevance 0.16

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