Abstract:
:Interleukin-1 beta stimulates corticotropin-releasing factor (CRF) secretion from the hypothalamus involving the activation of prostaglandins. This study investigated the possibility that nitric oxide (NO) acts as a mediator of interleukin-1-induced CRF release. An in vitro rat hypothalami continuous perifusion system was used. Pre- and co-incubation of hypothalami with either the NO synthase inhibitor, NG-nitro-L-arginine (1 mM), or the NO scavenger, hemoglobin (10 microM), induced a marked reduction in the effect of interleukin-1 (3 pM) on CRF secretion. The effect of NG-nitro-L-arginine was prevented by pre-exposure of hypothalami to L-arginine (1 mM). We also studied whether the involvement of NO in this interleukin-1 effect could involve a prostaglandin action. The concurrent treatment with NG-nitro-L-arginine and indomethacin (14 microM)--an inhibitor of prostaglandin production--reduced interleukin-1-induced CRF release to the same level as NG-nitro-L-arginine alone, suggesting that prostaglandins might interact with NO on this interleukin-1 effect. These results suggest that NO plays a role in the in vitro stimulatory action of interleukin-1 on hypothalamic CRF secretion.
journal_name
Eur J Pharmacoljournal_title
European journal of pharmacologyauthors
Sandi C,Guaza Cdoi
10.1016/0014-2999(94)00700-hsubject
Has Abstractpub_date
1995-02-14 00:00:00pages
17-23issue
1-3eissn
0014-2999issn
1879-0712pii
0014-2999(94)00700-Hjournal_volume
274pub_type
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journal_title:European journal of pharmacology
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journal_title:European journal of pharmacology
pub_type: 杂志文章
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journal_title:European journal of pharmacology
pub_type: 杂志文章
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journal_title:European journal of pharmacology
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journal_title:European journal of pharmacology
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journal_title:European journal of pharmacology
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更新日期:1995-03-24 00:00:00
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journal_title:European journal of pharmacology
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journal_title:European journal of pharmacology
pub_type: 杂志文章,评审
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