INT7717
From wiki-pain
|
|
|
|
|
Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
These two drugs seem to require the alpha2A AR for spinal analgesia when given separately; when delivered as a combination, the resultant synergistic interaction requires the alpha2C AR as well.
| |||||||||||||||
| |||||||||||||||
|
The results suggest that alpha2-AR agonist-induced ventilatory excitation (tachypnea) requires the activation of alpha2A-ARs whereas clonidine-induced ventilatory depression (arrhythmic breathing) requires the activation of an alternate alpha2-AR subtype (presumably alpha2C-ARs). | |||||||||||||||
| |||||||||||||||
|
These data indicate that the enhancement of the pain threshold produced by amitriptyline and imipramine is mediated by activation of alpha2A-adrenoceptors. | |||||||||||||||
| |||||||||||||||
|
By means of quantitative real-time PCR we show that mRNAs encoding the alpha(2A)-adrenergic receptor (alpha(2A)AR) and the alpha(2C)-adrenergic receptor (alpha(2C)AR) are up-regulated in the brainstem, and that alpha(2C)AR mRNA is also elevated in the hippocampus and striatum of NET-KO mice. | |||||||||||||||
| |||||||||||||||
|
The endogenous catecholamines adrenaline and noradrenaline mediate their biological actions via activation of nine different adrenergic receptor subtypes, three alpha 1-receptors (alpha 1A, alpha 1B, alpha 1D), three alpha 2-receptors (alpha 2A, alpha 2B, alpha 2C) and three beta-receptors (beta 1, beta 2, beta 3). | |||||||||||||||
| |||||||||||||||
|
Transcutaneous electrical nerve stimulation activates peripherally located alpha-2A adrenergic receptors. | |||||||||||||||
| |||||||||||||||
|
We speculate that future development of agents capable of selectively activating the alpha2A-AR or blocking the alpha2B-AR may further improve our capability to treat hypertension, ischemic heart disease and heart failure. | |||||||||||||||
| |||||||||||||||
|
The animal experiments have led us to conclude that the sympathetic outflow is regulated by activation of the presynaptic alpha2A-AR subtype, which is the predominant alpha2-AR subtype in the central nervous system and exerts a sympathoinhibitory (hypotensive) action; on the contrary, activation of the central alpha2B-AR elicits a sympathoexcitatory response (such as seen in salt-induced hypertension, which requires functionally intact alpha2B-AR). | |||||||||||||||
| |||||||||||||||
|
These results indicate that stimulation of postsynaptic alpha 2-adrenoceptor, blockade of 5-HT2A receptors, or both, are involved in suppression of 5-HT2A receptor-mediated head-twitch response by mitragynine. | |||||||||||||||
| |||||||||||||||
|
These two drugs seem to require the alpha2A AR for spinal analgesia when given separately; when delivered as a combination, the resultant synergistic interaction requires the alpha2C AR as well.
| |||||||||||||||
| |||||||||||||||
|
The results indicate that depression is associated with a selective increase in the high-affinity conformation of the brain alpha2A-adrenoceptors. | |||||||||||||||
| |||||||||||||||
|
These results indicate that clonidine and guanabenz impaired memory processes in a mouse passive avoidance paradigm through the selective activation of the alpha2A-adrenoceptor subtype. | |||||||||||||||
| |||||||||||||||
|
The studies employed two genetically engineered mouse strains, having either a targeted inactivation of the alpha2C-AR gene (alpha2C-KO) or over-expressing the alpha2C-AR (alpha2C-OE). | |||||||||||||||
| |||||||||||||||
|
The studies employed two genetically engineered mouse strains, having either a targeted inactivation of the alpha2C-AR gene (alpha2C-KO) or over-expressing the alpha2C-AR (alpha2C-OE). | |||||||||||||||
| |||||||||||||||
|
Selective increase of alpha2A-adrenoceptor agonist binding sites in brains of depressed suicide victims. | |||||||||||||||
| |||||||||||||||
|
The analgesic efficacy of partial opioid agonists is increased in mice with targeted inactivation of the alpha2A-adrenoceptor gene. | |||||||||||||||
| |||||||||||||||
|
Norepinephrine transporter knockout-induced up-regulation of brain alpha2A/C-adrenergic receptors. | |||||||||||||||
| |||||||||||||||
|
The animal experiments have led us to conclude that the sympathetic outflow is regulated by activation of the presynaptic alpha2A-AR subtype, which is the predominant alpha2-AR subtype in the central nervous system and exerts a sympathoinhibitory (hypotensive) action; on the contrary, activation of the central alpha2B-AR elicits a sympathoexcitatory response (such as seen in salt-induced hypertension, which requires functionally intact alpha2B-AR). | |||||||||||||||
| |||||||||||||||
|
The effects of prazosin and yohimbine on the vasopressor response to sympathetic nerve stimulation, and to i.v. administration of norepinephrine were studied in the pithed rat to ascertain whether prazosin and yohimbine would preferentially block pressure responses due to exogenous versus endogenous alpha-adrenergic receptor activation. | |||||||||||||||
| |||||||||||||||
|
The animal experiments have led us to conclude that the sympathetic outflow is regulated by activation of the presynaptic alpha2A-AR subtype, which is the predominant alpha2-AR subtype in the central nervous system and exerts a sympathoinhibitory (hypotensive) action; on the contrary, activation of the central alpha2B-AR elicits a sympathoexcitatory response (such as seen in salt-induced hypertension, which requires functionally intact alpha2B-AR). | |||||||||||||||
| |||||||||||||||
|
General Comments
This test has worked.