Mastrangelo D, Mathison R, Huggel H
Pharmacology. 1983;27(6):305-18. doi: 10.1159/000137885.
A dose-dependent contractile effect of substance P (SP) on the isolated, everted rat portal vein was competitively inhibited by two selective SP antagonists (pro2, phe7, trp9)-SP and (pro4, trp7,9)-SP 4-11. Phentolamine, atropine, methysergide, mepyramine, cimetidine, Sar1, Ile8-angiotensin II, Leu8, des-Arg9-bradykinin and indomethacin did not block the action of SP. However, some of these antagonists differentially reduced SP responses, but such inhibitory effects were shown to be nonspecific. The results suggest that the SP-induced contractions of the rat portal vein were directly mediated by specific receptors localized on the smooth muscle cells. In addition, the response to SP appeared to be independent of prostaglandin biosynthesis.
P物质(SP)对离体翻转大鼠门静脉的剂量依赖性收缩作用被两种选择性SP拮抗剂(脯氨酸2、苯丙氨酸7、色氨酸9)-SP和(脯氨酸4、色氨酸7、9)-SP 4-11竞争性抑制。酚妥拉明、阿托品、麦角新碱、甲氧苄啶、西咪替丁、Sar1、Ile8-血管紧张素II、Leu8、去-Arg9-缓激肽和吲哚美辛均不能阻断SP的作用。然而,其中一些拮抗剂可不同程度地降低SP反应,但这种抑制作用显示为非特异性的。结果表明,SP诱导的大鼠门静脉收缩是由位于平滑肌细胞上的特异性受体直接介导的。此外,对SP的反应似乎与前列腺素生物合成无关。