一氧化氮是速激肽NK3受体诱导大鼠肠系膜动脉舒张的介质。
Nitric oxide is a mediator of tachykinin NK3 receptor-induced relaxation in rat mesenteric artery.
作者信息
Mizuta A, Takano Y, Honda K, Saito R, Matsumoto T, Kamiya H
机构信息
Department of Pharmacology, Faculty of Pharmaceutical Sciences, Fukuoka University, Japan.
出版信息
Br J Pharmacol. 1995 Dec;116(7):2919-22. doi: 10.1111/j.1476-5381.1995.tb15945.x.
Abstract
- 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(-5) M), 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. N omega-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.
摘要
- 在大鼠离体肠系膜动脉中研究了速激肽诱导血管舒张的机制。2. 选择性NK3激动剂senktide可引起由去氧肾上腺素（10⁻⁵ M）预收缩的动脉产生有效的内皮依赖性舒张，但NK1激动剂则不能。3. 非肽类NK3拮抗剂SR 142801可抑制senktide诱导的舒张。然而，非肽类NK1拮抗剂CP-96,345和基于肽的NK2拮抗剂L-659,877对senktide诱导的舒张没有影响。4. 一氧化氮合成抑制剂Nω-硝基-L-精氨酸（L-NOARG）显著减弱了对senktide的舒张反应。5. 这些结果表明，大鼠肠系膜动脉内皮细胞具有速激肽NK3受体，且NK3激动剂诱导的血管舒张是由内皮细胞释放一氧化氮（NO）介导的。
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