Stimulation of nitric oxide release from rat spinal cord by prostaglandin E 2

We recently demonstrated that intrathecal administration of prostaglandin E 2 (PGE 2 ) and PGF 2α induced allodynia through a pathway that includes the glutamate receptor and nitric oxide (NO)‐generating systems from pharmacological studies. In order to clarify the involvement of NO in prostaglandin...

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Bibliographic Details
Published in:British journal of pharmacology 2009-02, Vol.123 (5), p.890-894
Main Authors: Sakai, Masato, Minami, Toshiaki, Hara, Naoki, Nishihara, Isao, Kitade, Hiroaki, Kamiyama, Yasuo, Okuda, Kazuyuki, Takahashi, Hakuo, Mori, Hidemaro, Ito, Seiji
Format: Article
Language:English
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Summary:We recently demonstrated that intrathecal administration of prostaglandin E 2 (PGE 2 ) and PGF 2α induced allodynia through a pathway that includes the glutamate receptor and nitric oxide (NO)‐generating systems from pharmacological studies. In order to clarify the involvement of NO in prostaglandin‐induced allodynia, we measured NO released from rat spinal cord slices by a chemiluminescence method. PGE 2 stimulated NO release from both dorsal and ventral regions all along the spinal cord. PGE 2 stimulated the release within 10 min and increased it in a time‐dependent manner. The PGE 2 ‐induced NO release was observed at 100 n M –10 μ M . PGF 2α stimulated the release at concentrations higher than 1 μ M , but PGD 2 (up to 10 μ M ) did not enhance it. 17‐Phenyl‐ω‐trinor PGE 2 (EP 1 >EP 3 ) and sulprostone (EP 1
ISSN:0007-1188
1476-5381
DOI:10.1038/sj.bjp.0701661