INT3722

Context Info Confidence 0.42 First Reported 1977 Last Reported 2010 Negated 0 Speculated 0 Reported most in Abstract Documents 19 Total Number 20 Disease Relevance 4.88 Pain Relevance 4.21

cytosol (Acot1) mitochondrion (Acot1) lipid metabolic process (Acot1) cytoplasm (Acot1)

Anatomy Link Frequency uterine smooth muscles 1 uterine muscles 1 brain 1 uterine 1 intestine 1 Acot1 (Mus musculus)

Pain Link Frequency Relevance Heat Neuronal nitric oxide synthase 1 99.84 tetrodotoxin 10 99.48 anesthesia 6 99.22 diclofenac 44 98.82 Clonidine 7 98.80 Dismenorea 3 98.72 acular 54 98.08 cerebral cortex 1 97.84 Neurotransmitter 2 97.24 tolerance 1 96.52

Disease Link Frequency Relevance Heat Cancer 19 99.86 Dysmenorrhea 3 98.72 Injury 32 95.20 Contracture 1 95.04 Disease 135 94.16 Carcinoma 13 90.04 Cognitive Disorder 10 88.92 Hypothermia 1 88.36 Body Weight 1 87.72 Parkinson's Disease 7 80.20

Sentences Mentioned In

Key:

Protein

Mutation

Event

Anatomy

Negation

Speculation

Pain term

Disease term

It is concluded that clonidine impairs the neuromuscular transmission by a noncompetitive blockade of ACh receptors, most likely affecting the ACh channel but not the recognition site of the ACh receptor.

Negative_regulation (blockade) of ACh associated with clonidine

1) Confidence 0.42 Published 1984 Journal Proc. Natl. Sci. Counc. Repub. China B Section Abstract Doc Link 6152843 Disease Relevance 0.10 Pain Relevance 0.56

During naturally occurring states of sleep and wakefulness, but not anesthesia, ODQ caused a significant (P < 0.001) decrease in ACh release.

Negative_regulation (decrease) of ACh associated with anesthesia

2) Confidence 0.41 Published 2006 Journal J. Appl. Physiol. Section Abstract Doc Link 16424074 Disease Relevance 0 Pain Relevance 0.41

It is postulated that the decrease in Ach content is due to an increased release of acetylcholine as a result of development of tolerance to morphine.

Negative_regulation (decrease) of Ach associated with tolerance and morphine

3) Confidence 0.38 Published 1977 Journal Arch Int Pharmacodyn Ther Section Abstract Doc Link 849063 Disease Relevance 0.18 Pain Relevance 0.40

These results indicate that the blocking effect of beta-eudesmol on nerve-evoked contraction, was due to blockade of nicotinic ACh receptor channels at the neuromuscular junction.

Negative_regulation (blockade) of ACh receptor in nerve

4) Confidence 0.37 Published 1991 Journal Neuropharmacology Section Abstract Doc Link 1780041 Disease Relevance 0.05 Pain Relevance 0.09

Dialysis delivery of tetrodotoxin to the PnO significantly decreased ACh by 58% below control levels, confirming that measured ACh reflected neurotransmitter release.

Negative_regulation (decreased) of ACh associated with tetrodotoxin and neurotransmitter

5) Confidence 0.37 Published 2004 Journal Neuroscience Section Abstract Doc Link 15207318 Disease Relevance 0 Pain Relevance 0.34

Following this expansion of the S3 ACh content, veratridine caused an even greater loss of S3 ACh, and increased the Ca2+-independent release of ACh slightly.

Negative_regulation (loss) of ACh

6) Confidence 0.36 Published 1984 Journal Brain Res. Section Abstract Doc Link 6697191 Disease Relevance 0 Pain Relevance 0.09

Like phencyclidine, beta-eudesmol blocked the nicotinic ACh receptor channel in both the open and closed conformations, and accelerated the desensitization of the nicotinic ACh receptor.

Negative_regulation (blocked) of ACh receptor

7) Confidence 0.32 Published 1991 Journal Neuropharmacology Section Abstract Doc Link 1780041 Disease Relevance 0 Pain Relevance 0.04

The results showed that all the three extracts inhibited the automatic contraction and Ach, BaCl2-induced spasmodic contraction of isolated rabbit intestine, among the three extracts the volatile oil was the most potent.

Negative_regulation (inhibited) of Ach in intestine

8) Confidence 0.27 Published 1998 Journal Zhong Yao Cai Section Abstract Doc Link 12569839 Disease Relevance 0.06 Pain Relevance 0

Decreased ACh levels caused by infusion of HC-3 or tetrodotoxin (TTX) were accompanied by increased levels of free choline.

Negative_regulation (Decreased) of ACh associated with tetrodotoxin

9) Confidence 0.25 Published 2008 Journal Neurochem. Int. Section Abstract Doc Link 18023504 Disease Relevance 0 Pain Relevance 0.17

Furthermore, induction of pregnancy in tumor bearing animals reduces the responsiveness of uterine smooth muscles to oxytocin and ACh.

Negative_regulation (reduces) of ACh in uterine smooth muscles associated with cancer

10) Confidence 0.19 Published 1998 Journal J. Exp. Clin. Cancer Res. Section Abstract Doc Link 9894759 Disease Relevance 0.93 Pain Relevance 0.10

The results of the present study indicate that the presence of tumor cells decreases the responses of the uterine smooth muscles to oxytocin and ACh, while pregnancy increases the uterine contractions induced by oxytocin and ACh.

Negative_regulation (decreases) of ACh in uterine associated with cancer and dismenorea

11) Confidence 0.19 Published 1998 Journal J. Exp. Clin. Cancer Res. Section Abstract Doc Link 9894759 Disease Relevance 0.90 Pain Relevance 0.10

In AChE-/- mice, calcium-free conditions reduced hippocampal ACh levels by 50%, and infusion of tetrodotoxin by more than 90%, indicating continuous ACh release.

Negative_regulation (reduced) of ACh associated with tetrodotoxin

12) Confidence 0.13 Published 2007 Journal J. Neurochem. Section Abstract Doc Link 17212694 Disease Relevance 0.32 Pain Relevance 0.15

In tumor bearing mice, the induction of pregnancy significantly reduced the sensitivity of the uterine smooth muscles to oxytocin and ACh when compared with the uterine muscles obtained from pregnant non-tumor bearing mice.

Negative_regulation (reduced) of ACh in uterine muscles associated with cancer

13) Confidence 0.08 Published 1998 Journal J. Exp. Clin. Cancer Res. Section Abstract Doc Link 9894759 Disease Relevance 0.93 Pain Relevance 0.08

We evaluated the effects of superfusing 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ), eNOS null (B) an inhibitor of soluble guanylyl cyclase, and 7-nitroindazole sodium (7-NI), a selective neuronal nitric oxide synthase (nNOS) inhibitor, on the acetylcholine (ACh) response in endothelial NOS (eNOS) null mice.

Negative_regulation (inhibitor) of ACh in neuronal associated with neuronal nitric oxide synthase

14) Confidence 0.08 Published 1998 Journal Am. J. Physiol. Section Abstract Doc Link 9486242 Disease Relevance 0.07 Pain Relevance 0.14

When cells were grown in medium containing reduced Ca2+, the total number of AChRs was decreased by 20-50%.

Negative_regulation (number) of AChRs

15) Confidence 0.03 Published 1983 Journal Exp. Cell Res. Section Abstract Doc Link 6617773 Disease Relevance 0 Pain Relevance 0.28

When cells were grown in medium containing reduced Ca2+, the total number of AChRs was decreased by 20-50%.

Negative_regulation (decreased) of AChRs

16) Confidence 0.03 Published 1983 Journal Exp. Cell Res. Section Abstract Doc Link 6617773 Disease Relevance 0 Pain Relevance 0.28

long-term inhibition of brain BChE and elevated extracellular ACh

Negative_regulation (inhibition) of ACh in brain

17) Confidence 0.02 Published 2006 Journal Journal of Biomedicine and Biotechnology Section Body Doc Link PMC1559913 Disease Relevance 1.06 Pain Relevance 0.17

In the ketorolac pretreated group (3 × 10-4 M), which was pretreated with 3AT, the relaxation was significantly decreased at ACh (10-7, 3 × 10-7 and 10-6 M) (P < 0.01; Fig. 4 and 5).

Negative_regulation (decreased) of ACh associated with acular

18) Confidence 0.01 Published 2010 Journal Korean Journal of Anesthesiology Section Body Doc Link PMC2946038 Disease Relevance 0.10 Pain Relevance 0.39

The relaxation of the diclofenac pretreated groups (10-4 and 3 × 10-4 M) was significantly decreased at ACh (10-7, 3 × 10-7 and 10-6 M), and the relaxation of the diclofenac pretreated groups (10-4 and 3 × 10-4 M) was significantly increased at ACh (10-7, 3 × 10-7 and 10-6 M), in proportion to the pretreatment concentration, after the ROS exposure, when compared with the relaxation of the diclofenac (10-5 M pretreated group) (P < 0.01, 0.01; Fig. 3).

Negative_regulation (decreased) of ACh associated with diclofenac

19) Confidence 0.01 Published 2010 Journal Korean Journal of Anesthesiology Section Body Doc Link PMC2946038 Disease Relevance 0.13 Pain Relevance 0.44

Both HeLa and 293T cells have been shown to lack AchRs[26], and several microarray analyses have failed to demonstrate AchR expression in 4T1 cells [52], [53], [54], consistent with lack of RVG binding to them.

Negative_regulation (lack) of AchRs in 4T1

20) Confidence 0.01 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2885418 Disease Relevance 0.07 Pain Relevance 0

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