INT49768

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Context Info
Confidence 0.41
First Reported 1995
Last Reported 2010
Negated 6
Speculated 1
Reported most in Body
Documents 58
Total Number 60
Disease Relevance 11.89
Pain Relevance 16.02

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

Anatomy Link Frequency
neurons 12
sensory neurons 3
visceral 2
neuronal 2
nerve 2
Kcnj5 (Rattus norvegicus)
Pain Link Frequency Relevance Heat
adenocard 297 100.00 Very High Very High Very High
Opioid 64 100.00 Very High Very High Very High
opioid receptor 273 99.92 Very High Very High Very High
addiction 40 99.92 Very High Very High Very High
Visceral pain 36 99.92 Very High Very High Very High
ischemia 100 99.50 Very High Very High Very High
noradrenaline 8 99.44 Very High Very High Very High
qutenza 7 99.34 Very High Very High Very High
Analgesic 137 99.24 Very High Very High Very High
Gabapentin 144 99.12 Very High Very High Very High
Disease Link Frequency Relevance Heat
Irritable Bowel Syndrome /

Irritable Bowel Syndrome Super / Visceral Pain

36 99.92 Very High Very High Very High
Shock 68 99.64 Very High Very High Very High
Cv Unclassified Under Development 102 99.50 Very High Very High Very High
Death 147 99.40 Very High Very High Very High
Reperfusion Injury 29 99.28 Very High Very High Very High
Arrhythmogenic Right Ventricular Dysplasia 5 99.12 Very High Very High Very High
Myocardial Infarction 29 98.98 Very High Very High Very High
Pressure Volume 2 Under Development 8 98.36 Very High Very High Very High
Nociception 155 98.16 Very High Very High Very High
Increased Venous Pressure Under Development 92 97.72 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
It has been argued that activation of KATP channels in the sarcolemmal membrane of heart muscle cells during ischemia provides an endogenous cardioprotective mechanism.
Positive_regulation (activation) of KATP in heart muscle cells associated with ischemia
1) Confidence 0.41 Published 2001 Journal Naunyn Schmiedebergs Arch. Pharmacol. Section Abstract Doc Link 11485036 Disease Relevance 0.40 Pain Relevance 0.20
We believe that stimulation of mu, delta, and kappa ORs increases myocardial tolerance to the arrhythmogenic effect of ischemia and reperfusion through activation of KATP channels.
Positive_regulation (activation) of KATP associated with ischemia, tolerance and arrhythmogenic right ventricular dysplasia
2) Confidence 0.38 Published 2003 Journal Izv. Akad. Nauk. Ser. Biol. Section Abstract Doc Link 14994477 Disease Relevance 0.81 Pain Relevance 0.56
In conclusion, although there was little indication that it activates classical KATP channels in CA1 neurons, DZX strongly depresses several voltage-dependent, slowly inactivating outward and inward currents, which are important modulators of cell excitability.
Positive_regulation (activates) of KATP in neurons
3) Confidence 0.35 Published 1995 Journal Can. J. Physiol. Pharmacol. Section Abstract Doc Link 7585327 Disease Relevance 0.06 Pain Relevance 0.19
Thus, the purpose of the present study was to test the hypothesis that activation of opioid receptors mimics the cardioprotective effect of ischemic PC and that this effect is produced by activation of KATP channels in the rat heart.
Positive_regulation (activation) of KATP in heart associated with opioid receptor
4) Confidence 0.35 Published 1996 Journal Circ. Res. Section Abstract Doc Link 8635241 Disease Relevance 0.18 Pain Relevance 0.43
Halogenated inhalation anesthetics, such as isoflurane [19], sevoflurane [20], and deflurane [21] during ischemia-reperfusion injury, displays myocardial protection by activating the KATP ion channel; however, intravenous anesthetic such as propofol are known not to affect KATP ion channel, or to block, dose-dependently, KATP ion channel in higher concentrations [14].
Positive_regulation (activating) of KATP ion channel associated with reperfusion injury, ischemia and isoflurane
5) Confidence 0.35 Published 2010 Journal Korean Journal of Anesthesiology Section Body Doc Link PMC2872860 Disease Relevance 0.57 Pain Relevance 0.21
Our new observation adds sensory neurons as a site at which S-nitrosylation of cysteines on the KATP channel activates the KATP currents.
Positive_regulation (activates) of KATP in sensory neurons
6) Confidence 0.30 Published 2009 Journal Mol Pain Section Body Doc Link PMC2673211 Disease Relevance 0.06 Pain Relevance 0.04
Because the alkylating agent NEM directly interacts with this residue [59], it is likely that cysteine nitrosylation by NO modulates nucleotides-SUR1 interaction, resulting in allosteric activation of the KATP channel.
Positive_regulation (activation) of KATP
7) Confidence 0.30 Published 2009 Journal Mol Pain Section Body Doc Link PMC2673211 Disease Relevance 0.05 Pain Relevance 0.04
Our findings, along with previous studies, demonstrate that NO mediated activation of KATP channels might be employed as a pathway for therapy against pain.


Neg (NO) Positive_regulation (activation) of KATP associated with pain
8) Confidence 0.30 Published 2009 Journal Mol Pain Section Body Doc Link PMC2673211 Disease Relevance 0.25 Pain Relevance 0.43
However, our data show that an exogenous membrane permeable cGMP analogue still activates KATP channels via a PKG-dependent mechanism, as in other tissues [53,60].
Positive_regulation (activates) of KATP
9) Confidence 0.30 Published 2009 Journal Mol Pain Section Body Doc Link PMC2673211 Disease Relevance 0.08 Pain Relevance 0
CONCLUSIONS: Propofol had no effect on nicorandil induced sarcolemmal KATP channel activities in rat aortic smooth muscle cells, whereas thiamylal significantly inhibited these channel activities at clinically relevant concentrations.


Neg (no) Positive_regulation (induced) of KATP in smooth muscle cells
10) Confidence 0.30 Published 2005 Journal Masui Section Body Doc Link 15852621 Disease Relevance 0 Pain Relevance 0
Effects of inhibitors of the NO/cGMP/PKG pathway on NO-induced KATP channel activation
Positive_regulation (activation) of KATP
11) Confidence 0.22 Published 2009 Journal Mol Pain Section Body Doc Link PMC2673211 Disease Relevance 0 Pain Relevance 0
M) for 20 min failed to inhibit SNAP-induced KATP channel activation in both SS neurons (NPo 10 min after SNAP = 0.25 ± 0.09; n = 6; p = 1.0 vs. control) and SNL neurons (NPo 10 min after SNAP = 0.27 ± 0.16; n = 6; p = 1.0 vs. control; Figure 5A, B).
Positive_regulation (activation) of KATP in neurons
12) Confidence 0.22 Published 2009 Journal Mol Pain Section Body Doc Link PMC2673211 Disease Relevance 0 Pain Relevance 0
M), produced similar activation of KATP channels in both SS and SNL neuronal populations.
Positive_regulation (activation) of KATP in neuronal
13) Confidence 0.22 Published 2009 Journal Mol Pain Section Body Doc Link PMC2673211 Disease Relevance 0 Pain Relevance 0
M) for 20 min did not block SNAP-induced KATP channel activation in either SS neurons (NPo 10 min after SNAP = 0.14 ± 0.17; n = 5; p = 1.0 vs. control) or SNL neurons (NPo 10 min after SNAP = 0.26 ± 0.19; n = 6; p = 1.0 vs. control; Figure 5A, B).
Positive_regulation (activation) of KATP in neurons
14) Confidence 0.22 Published 2009 Journal Mol Pain Section Body Doc Link PMC2673211 Disease Relevance 0 Pain Relevance 0
To further investigate whether NO activates KATP currents via the classical NO/sGC/cGMP/PKG signaling pathway, we tested the effects of ODQ, a selective inhibitor of sGC, or the effects of KT 5823, a selective inhibitor of PKG, on SNAP-induced KATP channel activity in large SS or SNL DRG neurons, using the cell-attached patch-clamp configuration.
Positive_regulation (induced) of KATP in neurons
15) Confidence 0.22 Published 2009 Journal Mol Pain Section Body Doc Link PMC2673211 Disease Relevance 0 Pain Relevance 0
M) significantly activated KATP channels in either SS neurons (NPo value 5 min after application of 8-Br-cGMP = 0.22 ± 0.08; n = 8; p = 0.002 vs. baseline) or SNL (NPo = 0.17 ± 0.06; n = 7; p = 0.001 vs. baseline) neurons.
Positive_regulation (activated) of KATP in neurons
16) Confidence 0.22 Published 2009 Journal Mol Pain Section Body Doc Link PMC2673211 Disease Relevance 0 Pain Relevance 0
SNAP-induced KATP channel activation in SS neurons in the presence of 1 mM [ATP]i was completely reversed by subsequent bath application of DTT (5 mM) (n = 7, p = 0.009; Figure 7A).
Positive_regulation (induced) of KATP in neurons
17) Confidence 0.22 Published 2009 Journal Mol Pain Section Body Doc Link PMC2673211 Disease Relevance 0 Pain Relevance 0
These results suggest that NO activates KATP channels via mechanism(s) other than the NO/cGMP/PKG pathway.
Positive_regulation (activates) of KATP
18) Confidence 0.22 Published 2009 Journal Mol Pain Section Body Doc Link PMC2673211 Disease Relevance 0 Pain Relevance 0
If DRG neurons lack sGC and the capacity to mobilize the NO/sGC/cGMP pathway, it is likely that S-nitrosylation is the only mechanism by which NO activates KATP channels in these cells. nNOS expression in DRG neurons is markedly up-regulated after injury, especially in the small and medium sized neuronal population, enabling these neurons to produce endogenous NO [50,51].
Positive_regulation (activates) of KATP in neurons associated with injury
19) Confidence 0.22 Published 2009 Journal Mol Pain Section Body Doc Link PMC2673211 Disease Relevance 0.10 Pain Relevance 0.03
Pretreatment with KT 5823 significantly reduces 8-Br-cGMP-induced KATP channel activation in both SS neurons (n = 8; p < 0.001 vs. control) and SNL neurons (n = 6; p < 0.001 vs. control).
Positive_regulation (activation) of KATP in neurons
20) Confidence 0.22 Published 2009 Journal Mol Pain Section Body Doc Link PMC2673211 Disease Relevance 0 Pain Relevance 0

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