INT17857

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Context Info
Confidence 0.46
First Reported 1991
Last Reported 2010
Negated 0
Speculated 1
Reported most in Body
Documents 25
Total Number 26
Disease Relevance 21.16
Pain Relevance 2.45

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 (AGT) small molecule metabolic process (AGT) aging (AGT)
extracellular region (AGT) extracellular matrix organization (AGT) cell-cell signaling (AGT)
Anatomy Link Frequency
plasma 4
monocytes 3
blood 2
vascular system 2
Endothelium 2
AGT (Homo sapiens)
Pain Link Frequency Relevance Heat
bradykinin 51 98.20 Very High Very High Very High
Angina 30 97.12 Very High Very High Very High
Inflammation 121 95.20 Very High Very High Very High
Bioavailability 4 92.40 High High
b2 receptor 2 91.44 High High
antagonist 56 86.88 High High
ischemia 28 83.76 Quite High
cva 76 81.76 Quite High
fibrosis 5 78.64 Quite High
Neurotransmitter 3 78.40 Quite High
Disease Link Frequency Relevance Heat
Increased Venous Pressure Under Development 263 100.00 Very High Very High Very High
Adhesions 55 100.00 Very High Very High Very High
Cv Unclassified Under Development 27 99.88 Very High Very High Very High
Proteinuria 10 99.64 Very High Very High Very High
Stress 37 99.56 Very High Very High Very High
Natriuresis 20 99.32 Very High Very High Very High
Apoptosis 30 98.76 Very High Very High Very High
Diabetes Mellitus 286 98.52 Very High Very High Very High
Disease 48 98.00 Very High Very High Very High
Myocardial Infarction 206 97.80 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Atenolol reduces renin secretion from the renin-angiotensin system and consequently decreases the production of angiotensin II and plasma aldosterone.
Negative_regulation (decreases) of Gene_expression (production) of angiotensin II in plasma
1) Confidence 0.46 Published 1998 Journal Drugs Section Abstract Doc Link 9813739 Disease Relevance 0.72 Pain Relevance 0.16
Blockade of the renin-angiotensin system plus calcium entry blockade or diuretic therapy
Negative_regulation (Blockade) of Gene_expression (system) of angiotensin
2) Confidence 0.41 Published 2009 Journal Vascular Health and Risk Management Section Body Doc Link PMC2672450 Disease Relevance 0.20 Pain Relevance 0
Blockade of the renin-angiotensin system plus calcium entry blockade or diuretic therapy
Negative_regulation (blockade) of Gene_expression (system) of angiotensin
3) Confidence 0.41 Published 2009 Journal Vascular Health and Risk Management Section Body Doc Link PMC2672450 Disease Relevance 0.20 Pain Relevance 0
There is large evidence from animal and human studies that inhibition of the renin–angiotensin system reduces proteinuria.35,36
Negative_regulation (inhibition) of Gene_expression (system) of angiotensin associated with proteinuria
4) Confidence 0.39 Published 2009 Journal Vascular Health and Risk Management Section Body Doc Link PMC2788599 Disease Relevance 1.24 Pain Relevance 0
In addition to a decrease in production or an increase in degradation of NO, resulting in deficiency of NO activity, there can be an imbalance between endothelium-produced vasodilator factors (i.e., prostacyclin, NO) and vasoconstrictor factors (i.e., endothelin, angiotensin II) that favors the latter.46) NO is known to suppress production of endothelin-1 and angiotensin II, which are potent vasoconstrictors and proliferators of vascular smooth muscle, and deficiency of NO may enhance synthesis of these vasoconstrictors.47)48) Endothelium also produces vasodilators, such as prostacyclin49) or hyperpolarizing factor,50) and vasoconstrictors, such as endothelins51) or endithelium-dependent constricting factors.52) Therefore, it is possible that decrease of vasodilators or increase of vasoconstrictors may also be involved in pathogenesis of vasospastic angina.


Negative_regulation (suppress) of Gene_expression (production) of angiotensin II in Endothelium associated with cva
5) Confidence 0.13 Published 2009 Journal Korean Circulation Journal Section Body Doc Link PMC2801457 Disease Relevance 0.58 Pain Relevance 0.23
ACE inhibitors reduce biosynthesis of angiotensin II whereas ARBs completely block AT1 receptors, and both are effective antihypertensive agents.
Negative_regulation (reduce) of Gene_expression (biosynthesis) of angiotensin II
6) Confidence 0.11 Published 2010 Journal Indian Journal of Pharmacology Section Body Doc Link PMC2937316 Disease Relevance 0.98 Pain Relevance 0.13
Therefore, blocking the generation of angiotensin-II or inhibiting its binding to specific receptors may decrease the subsequent risk for unstable angina and acute myocardial infarction.
Negative_regulation (inhibiting) of Gene_expression (generation) of angiotensin-II associated with angina and myocardial infarction
7) Confidence 0.10 Published 2000 Journal Curr. Opin. Cardiol. Section Abstract Doc Link 10952419 Disease Relevance 0.69 Pain Relevance 0.10
This greater reduction in the mean diastolic BP associated with telmisartan might be due to the selective blockade of the angiotensin II AT1 receptor so that the actions of angiotensin II produced by the alternative pathway are also blocked.
Negative_regulation (blocked) of Gene_expression (produced) of angiotensin II
8) Confidence 0.08 Published 2010 Journal Indian Journal of Pharmacology Section Body Doc Link PMC2937316 Disease Relevance 0.26 Pain Relevance 0.04
ACE inhibitors act by reducing the biosynthesis of angiotensin II by blocking the action of ACE on angiotensin I but do not inhibit the alternative non-ACE angiotensin II generating pathways whereas ARBs block the AT1 receptor-mediated actions of angiotensin II without inhibiting the synthesis of angiotensin II.
Negative_regulation (inhibiting) of Gene_expression (synthesis) of angiotensin II
9) Confidence 0.08 Published 2010 Journal Indian Journal of Pharmacology Section Body Doc Link PMC2937316 Disease Relevance 0.30 Pain Relevance 0
Angiotensin-converting enzyme inhibitors (ACEIs), by reducing the production of angiotensin II and possibly by blocking the degradation of bradykinin, exert many biological effects that lead to improvement in symptoms, fewer admissions to the hospital, and prolonged survival in HF; as a consequence, they are recommended for all patients with systolic dysfunction.
Negative_regulation (reducing) of Gene_expression (production) of angiotensin II associated with bradykinin and myocardial infarction
10) Confidence 0.07 Published 2010 Journal F1000 Med Rep Section Body Doc Link PMC2948383 Disease Relevance 1.39 Pain Relevance 0.10
Thus role of these ACE inhibitors is to inhibit the last step of the biosynthesis of angiotensin II and therefore causing a general vasodilatation and lowering of blood pressure [1â3].
Negative_regulation (inhibit) of Gene_expression (biosynthesis) of angiotensin II in blood associated with increased venous pressure under development
11) Confidence 0.06 Published 2010 Journal Scientia Pharmaceutica Section Body Doc Link PMC3007609 Disease Relevance 0.34 Pain Relevance 0.08
However, a significantly attenuated adrenergic responsiveness associated with incomplete blockade of the plasma renin-angiotensin system supports the hypothesis that inhibition of angiotensin II generation and of bradykinin degradation within the vascular wall mediates some of the vasodilatory effects of ACE inhibitors.


Negative_regulation (inhibition) of Gene_expression (generation) of angiotensin II in plasma
12) Confidence 0.06 Published 1996 Journal Anesthesiology Section Body Doc Link 8638832 Disease Relevance 0 Pain Relevance 0
Angiotensin converting enzyme inhibitor therapy decreases the production of the vasoconstrictive angiotensin II and reduces the degradation of certain kinines of vasodilatator action.
Negative_regulation (decreases) of Gene_expression (production) of angiotensin II
13) Confidence 0.06 Published 1991 Journal Ther Hung Section Abstract Doc Link 1948779 Disease Relevance 0.41 Pain Relevance 0.06
Inhibition of rennin angiotensin pathway (Table 2A)
Negative_regulation (Inhibition) of Gene_expression (pathway) of angiotensin
14) Confidence 0.06 Published 2007 Journal Vascular Health and Risk Management Section Body Doc Link PMC2350146 Disease Relevance 0.90 Pain Relevance 0.05
Both agents can reduce the expression of angiotensin I and II receptors on endothelial cells and monocytes.
Negative_regulation (reduce) of Gene_expression (expression) of angiotensin I in monocytes
15) Confidence 0.05 Published 2009 Journal Vascular Health and Risk Management Section Body Doc Link PMC2762434 Disease Relevance 1.18 Pain Relevance 0.17
They are capable of producing vasodilatation by virtue of inhibiting the production of angiotensin II, degradation of natriuretic peptides and bradykinin.
Negative_regulation (inhibiting) of Gene_expression (production) of angiotensin associated with natriuresis, increased venous pressure under development and bradykinin
16) Confidence 0.05 Published 2003 Journal Drugs Section Abstract Doc Link 14498755 Disease Relevance 1.16 Pain Relevance 0.05
Inhibition by indomethacin of angiotensin II and thromboxane A(2) synthesis may, during exercise, counterbalance renal vasoconstriction caused by blockade of vasodilatory prostaglandins.
Negative_regulation (Inhibition) of Gene_expression (synthesis) of angiotensin II associated with increased venous pressure under development
17) Confidence 0.04 Published 1999 Journal Clin. Sci. Section Abstract Doc Link 10491346 Disease Relevance 0.17 Pain Relevance 0.11
ACE inhibitors reduce production of angiotensin II, which prevents vasoconstriction, reduces adhesion molecules and growth factors, decreases oxidative stress and prevents apoptosis.
Negative_regulation (decreases) of Gene_expression (production) of angiotensin II associated with stress, apoptosis, increased venous pressure under development and adhesions
18) Confidence 0.04 Published 2009 Journal Drugs Section Abstract Doc Link 19275271 Disease Relevance 1.48 Pain Relevance 0.09
ACE inhibitors reduce production of angiotensin II, which prevents vasoconstriction, reduces adhesion molecules and growth factors, decreases oxidative stress and prevents apoptosis.
Negative_regulation (reduces) of Gene_expression (production) of angiotensin II associated with stress, apoptosis, increased venous pressure under development and adhesions
19) Confidence 0.04 Published 2009 Journal Drugs Section Abstract Doc Link 19275271 Disease Relevance 1.46 Pain Relevance 0.09
The mechanisms underlying the beneficial effects of ACE inhibition are complex, and include inhibition of angiotensin II production with, subsequently, a reduction of its negative effects on the vascular system.
Negative_regulation (inhibition) of Gene_expression (production) of angiotensin II in vascular system
20) Confidence 0.04 Published 2007 Journal Cardiovasc Drugs Ther Section Body Doc Link PMC2039813 Disease Relevance 0.81 Pain Relevance 0.08

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