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Nitric oxide is a mediator of tachykinin NK 3 receptor‐induced relaxation in rat mesenteric artery
Author(s) -
Mizuta Aki,
Takano Yukio,
Honda Kenji,
Saito Ryo,
Matsumoto Takafumi,
Kamiya HiroO
Publication year - 1995
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1995.tb15945.x
Subject(s) - agonist , nitric oxide , tachykinin receptor , vasodilation , phenylephrine , nk1 receptor antagonist , endocrinology , medicine , mesenteric arteries , antagonist , chemistry , substance p , endothelium , nitric oxide synthase , receptor , pharmacology , artery , neuropeptide , blood pressure
1 The mechanism of vasodilatation induced by tachykinin peptides was studied in isolated mesenteric arteries of rats. 2 Senktide, a selective NK 3 agonist, elicited potent endothelium‐dependent relaxation of arteries precontracted with phenylephrine (10‐ 5 m), but an NK 1 agonist did not. 3 A non‐peptide NK 3 antagonist, SR 142801, inhibited senktide‐induced relaxation. However, a non‐peptide NK 1 antagonist, CP‐96,345, and a peptide‐based NK 2 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 NK 3 receptors, and that NK 3 agonist‐induced vasodilatation is mediated by release of nitric oxide (NO) from the endothelium.