Nitric oxide is a mediator of tachykinin NK3 receptor‐induced relaxation in rat mesenteric artery

1 The mechanism of vasodilatation induced by tachykinin peptides was studied in isolated mesenteric arteries of rats. 2 Senktide, a selective NK3 agonist, elicited potent endothelium‐dependent relaxation of arteries precontracted with phenylephrine (10‐5m), but an NK1 agonist did not. 3 A non‐peptid...

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Published inBritish journal of pharmacology Vol. 116; no. 7; pp. 2919 - 2922
Main Authors Mizuta, Aki, Takano, Yukio, Honda, Kenji, Saito, Ryo, Matsumoto, Takafumi, Kamiya, Hiro‐O
Format Journal Article
LanguageEnglish
Published Oxford, UK Blackwell Publishing Ltd 01.12.1995
Nature Publishing
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Summary:1 The mechanism of vasodilatation induced by tachykinin peptides was studied in isolated mesenteric arteries of rats. 2 Senktide, a selective NK3 agonist, elicited potent endothelium‐dependent relaxation of arteries precontracted with phenylephrine (10‐5m), but an NK1 agonist did not. 3 A non‐peptide NK3 antagonist, SR 142801, inhibited senktide‐induced relaxation. However, a non‐peptide NK1 antagonist, CP‐96,345, and a peptide‐based NK2 antagonist, L‐659,877, had no effect on senktide‐induced relaxation. 4 Nω‐nitro‐L‐arginine (l‐NOARG), a nitric oxide synthesis inhibitor, markedly attenuated the relaxant response to senktide. 5 These results suggest that the endothelium of rat mesenteric arteries possesses tachykinin NK3 receptors, and that NK3 agonist‐induced vasodilatation is mediated by release of nitric oxide (NO) from the endothelium.
Bibliography:Exploratory Research Lab., Dainippon Pharmaceut. Co., Ltd., Osaka 564, Japan.
ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:0007-1188
1476-5381
DOI:10.1111/j.1476-5381.1995.tb15945.x