INT19302

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Context Info
Confidence 0.79
First Reported 1988
Last Reported 2010
Negated 0
Speculated 0
Reported most in Abstract
Documents 31
Total Number 31
Disease Relevance 3.39
Pain Relevance 6.92

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

signal transduction (OXT) extracellular space (OXT) extracellular region (OXT)
response to stress (OXT) cytoplasm (OXT)
Anatomy Link Frequency
neurons 3
plasma 2
hypothalamus 2
body 2
bridge 1
OXT (Homo sapiens)
Pain Link Frequency Relevance Heat
Dopamine 2 100.00 Very High Very High Very High
Somatostatin 46 99.84 Very High Very High Very High
Endogenous opioid 22 99.82 Very High Very High Very High
agonist 72 99.68 Very High Very High Very High
Nicotine 20 99.68 Very High Very High Very High
narcan 81 99.46 Very High Very High Very High
tolerance 3 98.20 Very High Very High Very High
Opioid 14 96.80 Very High Very High Very High
antagonist 8 96.52 Very High Very High Very High
Neuropeptide 288 95.60 Very High Very High Very High
Disease Link Frequency Relevance Heat
Pressure Volume 2 Under Development 34 99.56 Very High Very High Very High
Hypoglycemia 15 99.32 Very High Very High Very High
Pre-term Labor 69 98.44 Very High Very High Very High
Nicotine Addiction 21 92.12 High High
Premature Birth 42 91.24 High High
Natriuresis 16 84.48 Quite High
Dysmenorrhea 3 75.32 Quite High
Pressure And Volume Under Development 16 71.60 Quite High
Heart Rate Under Development 19 66.40 Quite High
Anxiety Disorder 2 62.48 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Endogenous opioids inhibit oxytocin release during nicotine-stimulated secretion of vasopressin in man.
Localization (release) of oxytocin associated with nicotine and endogenous opioid
1) Confidence 0.79 Published 1988 Journal Clin. Endocrinol. (Oxf) Section Title Doc Link 3214943 Disease Relevance 0.38 Pain Relevance 0.73
Naloxone abolishes the inhibiting effect of somatostatin on the release of oxytocin evoked by insulin-induced hypoglycemia in humans.
Localization (release) of oxytocin associated with hypoglycemia, somatostatin and narcan
2) Confidence 0.69 Published 1989 Journal Metab. Clin. Exp. Section Title Doc Link 2569658 Disease Relevance 0.34 Pain Relevance 0.94
Endogenous opioids do not play an important role in the suppression of OT release when AVP is secreted in response to an osmotic stimulus in man.
Localization (release) of OT associated with endogenous opioid
3) Confidence 0.67 Published 1989 Journal Clin. Endocrinol. (Oxf) Section Abstract Doc Link 2605788 Disease Relevance 0 Pain Relevance 0.45
We conclude that endogenous opioid peptides do not modulate OT release during breast feeding or breast stimulation in women.
Localization (release) of OT associated with endogenous opioid
4) Confidence 0.59 Published 1990 Journal Clin. Endocrinol. (Oxf) Section Abstract Doc Link 2401100 Disease Relevance 0 Pain Relevance 0.29
We have investigated the role of endogenous opioid peptides in the release of oxytocin (OT) in response to breast feeding and breast stimulation in humans.
Localization (release) of oxytocin associated with endogenous opioid
5) Confidence 0.59 Published 1990 Journal Clin. Endocrinol. (Oxf) Section Abstract Doc Link 2401100 Disease Relevance 0 Pain Relevance 0.21
We have investigated the role of endogenous opioid peptides in the release of oxytocin (OT) in response to breast feeding and breast stimulation in humans.
Localization (release) of OT associated with endogenous opioid
6) Confidence 0.59 Published 1990 Journal Clin. Endocrinol. (Oxf) Section Abstract Doc Link 2401100 Disease Relevance 0 Pain Relevance 0.21
Endogenous opioids inhibit the release of oxytocin (OT) when vasopressin (AVP) is secreted in response to acute pharmacological stimuli in man and to a variety of physiological and pharmacological stimuli to animals.
Localization (release) of OT associated with endogenous opioid
7) Confidence 0.59 Published 1989 Journal Clin. Endocrinol. (Oxf) Section Abstract Doc Link 2605788 Disease Relevance 0 Pain Relevance 0.33
Endogenous opioids inhibit the release of oxytocin (OT) when vasopressin (AVP) is secreted in response to acute pharmacological stimuli in man and to a variety of physiological and pharmacological stimuli to animals.
Localization (secreted) of OT associated with endogenous opioid
8) Confidence 0.59 Published 1989 Journal Clin. Endocrinol. (Oxf) Section Abstract Doc Link 2605788 Disease Relevance 0 Pain Relevance 0.41
Endogenous opioids inhibit the release of oxytocin (OT) when vasopressin (AVP) is secreted in response to acute pharmacological stimuli in man and to a variety of physiological and pharmacological stimuli to animals.
Localization (release) of oxytocin associated with endogenous opioid
9) Confidence 0.59 Published 1989 Journal Clin. Endocrinol. (Oxf) Section Abstract Doc Link 2605788 Disease Relevance 0 Pain Relevance 0.33
Endogenous opioids inhibit the release of oxytocin (OT) when vasopressin (AVP) is secreted in response to acute pharmacological stimuli in man and to a variety of physiological and pharmacological stimuli to animals.
Localization (secreted) of oxytocin associated with endogenous opioid
10) Confidence 0.59 Published 1989 Journal Clin. Endocrinol. (Oxf) Section Abstract Doc Link 2605788 Disease Relevance 0 Pain Relevance 0.41
The effect of somatostatin (SRIH) on the release of oxytocin (OT) in response to hypoglycemia during insulin tolerance test (ITT) was studied in seven normal men.
Localization (release) of oxytocin associated with hypoglycemia, tolerance and somatostatin
11) Confidence 0.53 Published 1989 Journal Metab. Clin. Exp. Section Abstract Doc Link 2569658 Disease Relevance 0.23 Pain Relevance 0.43
The effect of somatostatin (SRIH) on the release of oxytocin (OT) in response to hypoglycemia during insulin tolerance test (ITT) was studied in seven normal men.
Localization (release) of OT associated with hypoglycemia, tolerance and somatostatin
12) Confidence 0.53 Published 1989 Journal Metab. Clin. Exp. Section Abstract Doc Link 2569658 Disease Relevance 0.23 Pain Relevance 0.43
OT can induce dopamine release in ventromedial regions associated with reward [52] reinforcing generosity.
Localization (release) of OT associated with dopamine
13) Confidence 0.34 Published 2007 Journal PLoS ONE Section Body Doc Link PMC2040517 Disease Relevance 0.06 Pain Relevance 0.12
Naloxone increases the angiotensin II stimulated rise of arginine vasopressin and oxytocin secretion in man.
Localization (secretion) of oxytocin associated with narcan
14) Confidence 0.24 Published 1991 Journal Neuroendocrinology Section Title Doc Link 2041583 Disease Relevance 0 Pain Relevance 0.50
Previous studies in adult animals showed that hyperosmolality is a potent stimulus in the control of AVP and OT secretion [41-43].
Localization (secretion) of OT
15) Confidence 0.17 Published 2008 Journal BMC Dev Biol Section Body Doc Link PMC2570685 Disease Relevance 0.32 Pain Relevance 0.04
However, the results of pronounced pressor responses in the present as well as previous study [15] after the i.c.v. carbachol do not support the possibility that volume mechanisms may contribute to AVP and OT release by central cholinergic stimulation in utero.
Localization (release) of OT
16) Confidence 0.17 Published 2008 Journal BMC Dev Biol Section Body Doc Link PMC2570685 Disease Relevance 0.16 Pain Relevance 0.03
The hypothalamic-neurohypophysial system plays a fundamental role in the maintenance of body fluid homeostasis by secreting arginine vasopressin (AVP) and oxytocin (OT) in response to a variety of signals, including osmotic and nonosmotic stimuli.
Localization (secreting) of oxytocin in body
17) Confidence 0.15 Published 2008 Journal BMC Dev Biol Section Abstract Doc Link PMC2570685 Disease Relevance 0.07 Pain Relevance 0.07
This could be one of reasons why the released OT is relatively less than AVP under the same condition in the fetus compared to that in adults, indicting that fetal OT neurons showed a lower responsive ability in secretion or release of OT into the circulation from the fetal brain.
Localization (release) of OT in neurons
18) Confidence 0.15 Published 2008 Journal BMC Dev Biol Section Body Doc Link PMC2570685 Disease Relevance 0.34 Pain Relevance 0.03
Similar to AVP, the lack of change of the maternal plasma OT suggests that the increased fetal plasma OT is released from its own nerurohypophysis in response to central carbachol and fetal OT seems not pass the placental barrier to the maternal side.
Localization (released) of OT in plasma
19) Confidence 0.15 Published 2008 Journal BMC Dev Biol Section Body Doc Link PMC2570685 Disease Relevance 0 Pain Relevance 0.04
Consequently, unchanged fetal plasma osmolality and sodium levels make it unlikely that the central carbachol induced release of fetal AVP and OT was due to osmotic mechanisms.
Localization (release) of OT in plasma
20) Confidence 0.15 Published 2008 Journal BMC Dev Biol Section Body Doc Link PMC2570685 Disease Relevance 0.37 Pain Relevance 0.03

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