Abstract:
:The present study confirmed our previous assumption on the crucial role of central alpha2B-like adrenoceptor subtype in gastric mucosal defense. It was found that beside clonidine, rilmenidine, an alpha2/imidazoline receptor agonist and ST-91, an alpha2B-adrenoceptor preferring agonist inhibited the mucosal lesions induced by ethanol given intracerebroventricularly (i.c.v.). The ED50 values for clonidine, rilmenidine and ST-91 are 0.2, 0.01 and 16 nmol/rat i.c.v., respectively. The effect was reversed by the intracerebroventricularly injected alpha2B/2C-adrenoceptor antagonists prazosin and ARC-239, indicating the potential involvement of central alpha2B/2C-adrenoceptor subtype in the protective action. The gastroprotective effect of adrenoceptor stimulants was reversed by bilateral cervical vagotomy, suggesting that vagal nerve is likely to convey the central action to the periphery. In gastric mucosa both nitric oxide and prostaglandins may mediate the centrally-induced effect, since both indomethacin and N(G)-nitro-L-arginine reversed the protective effect of alpha2-adrenergic stimulants. Though expression of mRNA of alpha2B-, as well as alpha2A- and alpha2C-adrenoceptor subtypes was demonstrated in gastric mucosa of the rat, the hydrophilic ST-91, given peripherally (orally, subcutaneously), failed to exert mucosal protection, in contrast with clonidine and rilmenidine which were also effective. Consequently, while peripheral alpha2B-adrenoceptors are not likely to be involved in gastric mucosal protection, activation of central alpha2B-like adrenoceptor subtype may initiate a chain of events, which result in a vagal dependent gastroprotective action.
journal_name
Neurochem Intjournal_title
Neurochemistry internationalauthors
Gyires K,Zádori ZS,Shujaa N,Minorics R,Falkay G,Mátyus Pdoi
10.1016/j.neuint.2007.07.001subject
Has Abstractpub_date
2007-10-01 00:00:00pages
289-96issue
5eissn
0197-0186issn
1872-9754pii
S0197-0186(07)00195-7journal_volume
51pub_type
杂志文章abstract::Astrocytes can exocytotically release the transmitter glutamate. Increased cytosolic Ca(2+) concentration is necessary and sufficient in this process. The source of Ca(2+) for the Ca(2+)-dependent exocytotic release of glutamate from astrocytes predominately comes from endoplasmic reticulum (ER) stores with contributi...
journal_title:Neurochemistry international
pub_type: 杂志文章,评审
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journal_title:Neurochemistry international
pub_type: 杂志文章
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journal_title:Neurochemistry international
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journal_title:Neurochemistry international
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journal_title:Neurochemistry international
pub_type: 杂志文章,评审
doi:10.1016/j.neuint.2018.12.019
更新日期:2019-03-01 00:00:00
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journal_title:Neurochemistry international
pub_type: 杂志文章
doi:10.1016/j.neuint.2017.03.013
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journal_title:Neurochemistry international
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journal_title:Neurochemistry international
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journal_title:Neurochemistry international
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journal_title:Neurochemistry international
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journal_title:Neurochemistry international
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doi:10.1016/j.neuint.2007.06.001
更新日期:2008-01-01 00:00:00
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journal_title:Neurochemistry international
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journal_title:Neurochemistry international
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更新日期:1984-01-01 00:00:00
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更新日期:2004-04-01 00:00:00
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