INT291578

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Context Info
Confidence 0.03
First Reported 2010
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 1
Total Number 2
Disease Relevance 1.11
Pain Relevance 1.67

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

cytosol (Pde5a) signal transduction (Pde5a) mitochondrion (Pde12)
Anatomy Link Frequency
neurons 2
Pde12 (Rattus norvegicus)
Pde5a (Rattus norvegicus)
Pain Link Frequency Relevance Heat
gABA 22 98.68 Very High Very High Very High
potassium channel 6 98.48 Very High Very High Very High
Spinal nerve ligature 6 98.40 Very High Very High Very High
Neuropathic pain 38 98.32 Very High Very High Very High
antinociception 20 96.96 Very High Very High Very High
withdrawal 20 96.88 Very High Very High Very High
GABA receptor 20 95.52 Very High Very High Very High
Antinociceptive 10 94.00 High High
allodynia 14 71.68 Quite High
Hyperalgesia 10 71.12 Quite High
Disease Link Frequency Relevance Heat
Neuropathic Pain 58 98.32 Very High Very High Very High
Hyperalgesia 12 71.12 Quite High
Increased Venous Pressure Under Development 4 70.32 Quite High
Headache 2 63.00 Quite High
Post Operative Pain 2 61.96 Quite High
Diabetic Neuropathy 2 61.00 Quite High
Disease 4 59.88 Quite High
Injury 6 58.32 Quite High
Congenital Anomalies 2 57.64 Quite High
Pressure Volume 2 Under Development 2 37.36 Quite Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
It would therefore, appear that cGMP analog increases the synaptic GABA release to labeled paraventricular nucleus neurons.32,33 And increasing cGMP level by superfusing slices with another phosphodiesterase inhibitor (zaprinast) increases GABA release in the brain stem, while a guanylyl cyclase inhibitor (ODQ) reduces GABA release.15 Recently, it has been demonstrated that potassium channels are downstream effectors of cGMP on GABA release.33 Furthermore, the antinociception provoked by sildenafil and dibutyryl-cGMP was reversed by potassium channel blockers.10,34 These findings together suggest that intravenous sildenafil increases the cGMP level by inhibition of phosphodiesterase 5 and then induces the release of GABA through a downstream mechanism, involving potassium channels which act on GABA receptors, in turn leading to an antinociceptive effect.
Negative_regulation (inhibition) of phosphodiesterase 5 in neurons Positive_regulation (increases) of cGMP associated with antinociception, gaba, gaba receptor, potassium channel and antinociceptive
1) Confidence 0.03 Published 2010 Journal Yonsei Medical Journal Section Body Doc Link PMC2799976 Disease Relevance 0.07 Pain Relevance 0.82
Therefore, it is conceivable that the increased cGMP level by inhibition of phosphodiesterase 5 may contribute to the attenuation of the neuropathic pain at a systemic level.
Negative_regulation (inhibition) of phosphodiesterase 5 Positive_regulation (increased) of cGMP associated with neuropathic pain
2) Confidence 0.03 Published 2010 Journal Yonsei Medical Journal Section Body Doc Link PMC2799976 Disease Relevance 1.04 Pain Relevance 0.85

General Comments

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