Abstract:
:Potentiation by neuropeptide Y of serotonin (5-HT)-induced vasoconstriction was investigated in porcine coronary artery. 5-HT caused concentration-dependent contraction through 5-HT2A receptors. Neuropeptide Y (30 nM) significantly increased the 5HT-induced contraction by 16+/-5% in arteries with intact endothelium. Removal of the endothelium abolished the potentiation. A neuropeptide Y1 antagonist, BIBP3226, blocked this neuropeptide Y-induced potentiation. In vessels with intact endothelium, the potentiation by neuropeptide Y was inhibited by in the presence of a cyclo-oxygenase inhibitor, indomethacin (30 microM), but not by the presence of ETA or ETB endothelin receptor antagonists or an NO synthase inhibitor, NG-nitro-L-arginine (L-NNA) (1 mM) at all. A thromboxane A2 (TXA2) synthase inhibitor, ozagrel, and prostanoid TP receptor antagonists, seratrodast and ONO-3708, also inhibited the neuropeptide Y-induced potentiation. In the endothelium-denuded arteries, a prostanoid TP receptor agonist, U-46619 (0.01-0.1 nM), potentiated 5-HT-induced contraction. These results indicate that neuropeptide Y potentiates the 5-HT-induced contraction, due to release of TXA2 from the endothelium via neuropeptide Y1 receptors, in porcine coronary artery.
journal_name
Eur J Pharmacoljournal_title
European journal of pharmacologyauthors
Tsurumaki T,Nagai S,Bo X,Toyosato A,Higuchi Hdoi
10.1016/j.ejphar.2006.06.036subject
Has Abstractpub_date
2006-08-21 00:00:00pages
111-7issue
1-3eissn
0014-2999issn
1879-0712pii
S0014-2999(06)00654-6journal_volume
544pub_type
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journal_title:European journal of pharmacology
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