INT62349

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Context Info
Confidence 0.42
First Reported 1996
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 8
Total Number 8
Disease Relevance 6.47
Pain Relevance 1.86

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 (KNG1) extracellular region (KNG1) plasma membrane (KNG1)
Anatomy Link Frequency
plasma 2
vasculature 2
smooth muscle cells 2
vascular endothelium 2
KNG1 (Homo sapiens)
Pain Link Frequency Relevance Heat
bradykinin 64 100.00 Very High Very High Very High
adenocard 9 99.32 Very High Very High Very High
potassium channel 1 99.04 Very High Very High Very High
Catecholamine 5 97.52 Very High Very High Very High
Inflammation 10 91.68 High High
Glutamate 3 91.20 High High
Angina 13 73.92 Quite High
cINOD 2 58.40 Quite High
antagonist 21 37.80 Quite Low
ischemia 27 14.56 Low Low
Disease Link Frequency Relevance Heat
Apoptosis 69 99.36 Very High Very High Very High
Increased Venous Pressure Under Development 31 99.32 Very High Very High Very High
Stress 18 98.44 Very High Very High Very High
Atherosclerosis 69 97.60 Very High Very High Very High
Adhesions 7 96.16 Very High Very High Very High
Myocardial Infarction 148 95.48 Very High Very High Very High
Left Ventricular Hypertrophy 3 93.64 High High
INFLAMMATION 15 91.68 High High
Disease 15 90.92 High High
Drug Induced Neurotoxicity 3 90.36 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
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 Protein_catabolism (degradation) of bradykinin in plasma
1) Confidence 0.42 Published 1996 Journal Anesthesiology Section Body Doc Link 8638832 Disease Relevance 0 Pain Relevance 0
In animal models, ACE-I can retard the development of atherosclerosis, and these antiatherogenic properties can be related to the inhibition of angiotensin-II (Ang II) formation and to the inhibition of bradykinin degradation, which promotes vasodilatation by stimulating the production of arachidonic acid metabolites and nitric oxide (NO) in vascular endothelium.
Negative_regulation (inhibition) of Protein_catabolism (degradation) of bradykinin in vascular endothelium associated with atherosclerosis, increased venous pressure under development and bradykinin
2) Confidence 0.36 Published 2008 Journal Vascular Health and Risk Management Section Body Doc Link PMC2663435 Disease Relevance 0.98 Pain Relevance 0.19
ACE-I alter this balance by decreasing the formation of Ang II and the degradation of bradykinin (Figure 1): the bradykinin is potentiated and NO is released to a greater extent, resulting in decreased migration and proliferation of vascular smooth muscle cells, decreased accumulation and activation of inflammatory cells, decreased oxidative stress, and improved endothelial function.


Negative_regulation (decreasing) of Protein_catabolism (degradation) of bradykinin in smooth muscle cells associated with stress, inflammation and bradykinin
3) Confidence 0.36 Published 2008 Journal Vascular Health and Risk Management Section Body Doc Link PMC2663435 Disease Relevance 0.88 Pain Relevance 0.24
Inhibition of bradykinin degradation by ACE inhibitors may increase the activity of superoxide dismutase and modulate the production of nitric oxide, leading to the inactivation of reactive oxygen species, while also inhibiting various pro-oxidative mechanisms within the vasculature (Ehring et al 1994).
Negative_regulation (Inhibition) of Protein_catabolism (degradation) of bradykinin in vasculature associated with bradykinin
4) Confidence 0.12 Published 2007 Journal Clinical ophthalmology (Auckland, N.Z.) Section Body Doc Link PMC2701139 Disease Relevance 0.38 Pain Relevance 0.60
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 (blocking) of Protein_catabolism (degradation) of bradykinin associated with bradykinin and myocardial infarction
5) Confidence 0.11 Published 2010 Journal F1000 Med Rep Section Body Doc Link PMC2948383 Disease Relevance 1.39 Pain Relevance 0.11
Adenosine, acadesine, ACE inhibitors which prevent bradykinin degradation, nicorandil, and others have been used in clinical studies.
Negative_regulation (prevent) of Protein_catabolism (degradation) of bradykinin associated with adenocard and bradykinin
6) Confidence 0.10 Published 2007 Journal Vascular Health and Risk Management Section Body Doc Link PMC2291307 Disease Relevance 0.47 Pain Relevance 0.37
A concomitant decrease in the degradation of bradykinin as a result of ACE inhibition raises levels of this kinin, leading to vasodilation and an antiapoptotic action, as well as opposition of the negative actions of angiotensin II.
Negative_regulation (decrease) of Protein_catabolism (degradation) of bradykinin associated with increased venous pressure under development and bradykinin
7) Confidence 0.02 Published 2009 Journal Drugs Section Abstract Doc Link 19275271 Disease Relevance 1.44 Pain Relevance 0.09
ACE inhibitors work by inhibiting kininase II and degradation of bradykinin which results in elevated levels of bradykinin.
Negative_regulation (inhibiting) of Protein_catabolism (degradation) of bradykinin associated with bradykinin
8) Confidence 0.01 Published 2007 Journal Vascular Health and Risk Management Section Body Doc Link PMC2291334 Disease Relevance 0.93 Pain Relevance 0.27

General Comments

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