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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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
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container_title British journal of pharmacology
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creator Sakai, Masato
Minami, Toshiaki
Hara, Naoki
Nishihara, Isao
Kitade, Hiroaki
Kamiyama, Yasuo
Okuda, Kazuyuki
Takahashi, Hakuo
Mori, Hidemaro
Ito, Seiji
description 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
doi_str_mv 10.1038/sj.bjp.0701661
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The PGE 2 ‐evoked release was Ca 2+ ‐dependent and blocked by MK‐801 (NMDA receptor antagonist) and L ‐NAME (NO synthase inhibitor). The release was also inhibited by PGD 2 and dibutyryl‐cyclic AMP. The present study demonstrated that PGE 2 stimulates NO release in the rat spinal cord by activation of NMDA receptors through the EP 1 receptor, and supports our previous findings that the NO‐generating system is involved in the PGE 2 ‐induced allodynia. 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The PGE 2 ‐evoked release was Ca 2+ ‐dependent and blocked by MK‐801 (NMDA receptor antagonist) and L ‐NAME (NO synthase inhibitor). The release was also inhibited by PGD 2 and dibutyryl‐cyclic AMP. The present study demonstrated that PGE 2 stimulates NO release in the rat spinal cord by activation of NMDA receptors through the EP 1 receptor, and supports our previous findings that the NO‐generating system is involved in the PGE 2 ‐induced allodynia. 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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 &gt;EP 3 ) and sulprostone (EP 1 &lt;EP 3 ) were as potent as PGE 2 , but PGE 1 was less potent, in stimulating NO release. While M&amp;B 28767 (EP 3 ) did not enhance the release, butaprost (EP 2 ) stimulated it at 1 μ M . The PGE 2 ‐evoked release was blocked by ONO‐NT‐012, a bifunctional EP 1 antagonist/EP 3 agonist. The PGE 2 ‐evoked release was Ca 2+ ‐dependent and blocked by MK‐801 (NMDA receptor antagonist) and L ‐NAME (NO synthase inhibitor). The release was also inhibited by PGD 2 and dibutyryl‐cyclic AMP. The present study demonstrated that PGE 2 stimulates NO release in the rat spinal cord by activation of NMDA receptors through the EP 1 receptor, and supports our previous findings that the NO‐generating system is involved in the PGE 2 ‐induced allodynia. British Journal of Pharmacology (1998) 123 , 890–894; doi: 10.1038/sj.bjp.0701661</abstract><doi>10.1038/sj.bjp.0701661</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record>
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title Stimulation of nitric oxide release from rat spinal cord by prostaglandin E 2
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