INT183429

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Context Info
Confidence 0.56
First Reported 2005
Last Reported 2008
Negated 0
Speculated 0
Reported most in Body
Documents 5
Total Number 5
Disease Relevance 1.61
Pain Relevance 0.25

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)
Anatomy Link Frequency
myocytes 1
Pde5a (Rattus norvegicus)
Pain Link Frequency Relevance Heat
Angina 4 91.20 High High
ischemia 3 71.52 Quite High
antagonist 2 62.52 Quite High
Bioavailability 1 54.72 Quite High
Serotonin 1 47.16 Quite Low
Dopamine 1 46.60 Quite Low
Neurotransmitter 5 45.32 Quite Low
Central nervous system 1 42.92 Quite Low
adenocard 9 28.28 Quite Low
Inflammation 77 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Erectile Dysfunction 192 99.22 Very High Very High Very High
Natriuresis 8 96.96 Very High Very High Very High
Cv General 3 Under Development 6 91.20 High High
Reprotox - General 2 15 83.60 Quite High
Disease 28 79.68 Quite High
Hypertension 18 76.56 Quite High
Increased Venous Pressure Under Development 20 75.60 Quite High
Myocardial Infarction 3 73.36 Quite High
Diabetes Mellitus 46 72.96 Quite High
Cv Unclassified Under Development 11 71.52 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
On the other hand, various phosphodiesterases regulate cGMP catabolism, including PDE-5A, PDE-6, PDE-9A, PDE-10A, and PDE-11A according to their tissue specificity [21-23].
Localization (catabolism) of PDE-5A
1) Confidence 0.56 Published 2005 Journal BMC Pharmacol Section Body Doc Link PMC1131906 Disease Relevance 0.35 Pain Relevance 0.04
Whether the observed changes in the hormonal pattern may be attributed to the increased sexual activity, or directly due to the PDE5 inhibition (eg, NO stimulates hypothalamic gonadotropin-releasing hormone [Kohsaka et al 1999], and inhibits PRL release in rats [Velardez et al 2000]) remains to be determined.
Localization (release) of PDE5
2) Confidence 0.55 Published 2006 Journal Clinical Interventions in Aging Section Body Doc Link PMC2699638 Disease Relevance 0.50 Pain Relevance 0
It was later released in 1998 as the first oral treatment for ED, and this was followed in 2003 by the release of two more PDE5 inhibitors, vardenafil and tadalafil.


Localization (release) of PDE5 associated with erectile dysfunction
3) Confidence 0.42 Published 2008 Journal Therapeutics and Clinical Risk Management Section Body Doc Link PMC2643112 Disease Relevance 0.61 Pain Relevance 0.18
In mammals PDE4, PDE7 and PDE8 hydrolyze cAMP selectively, PDE5, PDE6, and PDE9 hydrolyse cGMP selectively and the remaining five PDEs (PDE1, 2, 3, 10, and 11) hydrolyze both cAMP and cGMP.
Localization (hydrolyse) of cGMP
4) Confidence 0.20 Published 2008 Journal International Journal of Chronic Obstructive Pulmonary Disease Section Body Doc Link PMC2650605 Disease Relevance 0 Pain Relevance 0
PDE4 is not inhibited by cGMP and thus originally PDE3 was called cGMP-inhibited PDE to distinguish it from PDE4. cGMP inhibition of PDE3 may be physiologically relevant to the elevation of cAMP levels in a variety of cells including human myocytes, where nitric oxide induced relaxation may be mediated by activation of guanylyl cyclase, elevation of intracellular cGMP levels and inhibition of PDE3 leading to elevated cAMP levels (Kirstein et al 1995).
Localization (called) of cGMP in myocytes
5) Confidence 0.20 Published 2008 Journal International Journal of Chronic Obstructive Pulmonary Disease Section Body Doc Link PMC2650605 Disease Relevance 0.16 Pain Relevance 0.03

General Comments

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