肺内动脉的内皮依赖性收缩：由内皮NK1受体和血栓素A2介导
Endothelium-dependent contraction in intrapulmonary arteries: mediation by endothelial NK1 receptors and TXA2.
作者信息
Shirahase H, Kanda M, Kurahashi K, Nakamura S, Usui H, Shimizu Y
机构信息
Pharmacology Division, Kyoto University, Japan.
出版信息
Br J Pharmacol. 1995 Aug;115(7):1215-20. doi: 10.1111/j.1476-5381.1995.tb15028.x.
Abstract
- We have examined whether three natural tachykinins, substance P (SP), neurokinin A (NKA) and neurokinin B (NKB) induce an endothelium-dependent contraction (EDC) in the rabbit isolated intrapulmonary artery. 2. Removal of the endothelium almost abolished the contraction induced by SP (10(-8) M) while it did not attenuate the contraction induced by SP (10(-7) M), NKA (10(-9) - 10(-7) M) or NKB (10(-8) and 10(-7) M). 3. The EDC induced by SP (10(-8) M) was abolished by NK1 antagonists (FK-888, CP-96345, CP-99994 and SR-140333) but not by an NK2 antagonist (SR-48968). 4. The EDC induced by SP was attenuated by cyclo-oxygenase inhibitors (aspirin and indomethacin), thromboxane A2 (TXA2) synthetase inhibitors (OKY-046, KY-234 and KY-063) and a TXA2 antagonist (S-1452). 5. The rank order of potency causing endothelium-independent contraction (EIC) was NKA > NKB > SP. The EIC induced by SP (10(-7) M) was attenuated by an NK2 antagonist but not by NK1 antagonists, cyclo-oxygenase inhibitors, TXA2 synthetase inhibitors or a TXA2 antagonist. 6. In conclusion, SP at 10(-8) M induces EDC via endothelial NK1 receptors and TXA2 production, and SP at 10(-7) M induces EIC via NK2 receptors in the rabbit intrapulmonary artery.
摘要
- 我们研究了三种天然速激肽，即P物质（SP）、神经激肽A（NKA）和神经激肽B（NKB）是否能在兔离体肺内动脉中诱导内皮依赖性收缩（EDC）。2. 去除内皮几乎消除了SP（10⁻⁸ M）诱导的收缩，而对SP（10⁻⁷ M）、NKA（10⁻⁹ - 10⁻⁷ M）或NKB（10⁻⁸和10⁻⁷ M）诱导的收缩没有减弱作用。3. SP（10⁻⁸ M）诱导的EDC被NK1拮抗剂（FK - 888、CP - 96345、CP - 99994和SR - 140333）消除，但不被NK2拮抗剂（SR - 48968）消除。4. SP诱导的EDC被环氧化酶抑制剂（阿司匹林和吲哚美辛）、血栓素A2（TXA2）合成酶抑制剂（OKY - 046、KY - 234和KY - 063）以及TXA2拮抗剂（S - 1452）减弱。5. 引起非内皮依赖性收缩（EIC）的效力顺序为NKA > NKB > SP。SP（10⁻⁷ M）诱导的EIC被NK2拮抗剂减弱，但不被NK1拮抗剂、环氧化酶抑制剂、TXA2合成酶抑制剂或TXA2拮抗剂减弱。6. 总之，10⁻⁸ M的SP通过内皮NK1受体和TXA2生成诱导EDC，而10⁻⁷ M的SP通过兔肺内动脉中的NK2受体诱导EIC。
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