INT135715

Context Info Confidence 0.42 First Reported 2005 Last Reported 2011 Negated 0 Speculated 0 Reported most in Body Documents 5 Total Number 5 Disease Relevance 1.70 Pain Relevance 0.56

extracellular space (Edn1) extracellular region (Edn1) cell-cell signaling (Edn1) cytoplasm (Edn1)

Anatomy Link Frequency endothelial cells 2 smooth muscle 2 endothelium 2 lung 2 Edn1 (Rattus norvegicus)

Pain Link Frequency Relevance Heat medulla 19 79.44 agonist 22 77.12 Calcitonin gene-related peptide 39 75.52 qutenza 14 75.36 Potency 3 70.96 antagonist 50 56.08 local anesthetic 7 50.00 Neurotransmitter 4 28.28 chemokine 3 19.72 adenocard 7 5.00

Disease Link Frequency Relevance Heat Diabetes Mellitus 132 96.76 Increased Venous Pressure Under Development 8 95.16 Renal Disease 8 90.32 Myocardial Infarction 21 89.96 Natriuresis 8 85.12 Stress 5 72.20 Pressure And Volume Under Development 9 65.52 Acute Decompensated Heart Failure (ADHF) 23 63.20 Syndrome 48 57.20 Apoptosis 3 52.56

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Key:

Protein

Mutation

Event

Anatomy

Negation

Speculation

Pain term

Disease term

Binding of Rh-ET-1 (16 nM) to smooth muscle (Fig. 6D) was reduced by BQ788 (1 µM; Fig. 6E) and was prevented by presence of either ET-1 (16 nM) or of both BQ788 (1 µM) and BQ123 (1 µM)[2] indicating selective binding to ETA- and ETB-receptors.

Negative_regulation (prevented) of Localization (presence) of ET-1 in smooth muscle

1) Confidence 0.42 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2879375 Disease Relevance 0 Pain Relevance 0.45

CONCLUSION: Bupivacaine and ropivacaine attenuated N-formyl-L-leucine-methionyl-L-phenylalanine-induced PAP, reduced lung edema, and diminished ET-1 release.

Negative_regulation (diminished) of Localization (release) of ET-1 in lung

2) Confidence 0.41 Published 2009 Journal Anesth. Analg. Section Body Doc Link 19690261 Disease Relevance 0 Pain Relevance 0

Although the mechanisms of ET-1 elevation during diabetes are relatively unknown, several research groups speculated that this increase could be due to an abnormal production by the affected endothelium [31] or lack of suppression of ET-1 release secondary to attenuated endothelium-derived relaxing factor production [32].

Negative_regulation (suppression) of Localization (release) of ET-1 in endothelium associated with diabetes mellitus

3) Confidence 0.37 Published 2005 Journal Cardiovasc Diabetol Section Body Doc Link PMC555576 Disease Relevance 0.76 Pain Relevance 0.08

RESULTS: Pretreatment with LAs significantly reduced the FMLP-induced PAP increase (treatment group v sham group: 0.5 to 5 mm Hg v 8 mm Hg; P < .05) and the release of endothelin-1 (2.4 v 5 fmol/mL).

Negative_regulation (reduced) of Localization (release) of endothelin-1

4) Confidence 0.17 Published 2006 Journal Reg Anesth Pain Med Section Body Doc Link 16701192 Disease Relevance 0 Pain Relevance 0

Whereas AII stimulates the release of ET 1, NO inhibits ET 1 release from endothelial cells.

Negative_regulation (inhibits) of Localization (release) of ET 1 in endothelial cells

5) Confidence 0.04 Published 2011 Journal International Journal of Nephrology Section Body Doc Link PMC2989717 Disease Relevance 0.94 Pain Relevance 0.03

General Comments

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