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通过刺激B1受体,des-Arg9-缓激肽使离体肠系膜动脉舒张。

Relaxation of isolated mesenteric arteries by des-Arg9-bradykinin stimulation of B1 receptors.

作者信息

Churchill L, Ward P E

出版信息

Eur J Pharmacol. 1986 Oct 14;130(1-2):11-8. doi: 10.1016/0014-2999(86)90178-0.

Abstract

The present studies were conducted to determine whether des-Arg-kinins can produce relaxation of isolated vessels. Both des-Arg9-bradykinin and bradykinin produced dose-dependent relaxations of isolated rabbit superior mesenteric arteries. Des-Arg9-bradykinin (ED50 = 7.2 X 10(-9) M) was 8.5 times more potent than bradykinin (ED50 = 6.1 X 10(-8) M). Des-Arg9-bradykinin-mediated relaxation was inhibited by the specific B1 receptor antagonist [Leu8]des-Arg9-bradykinin which produced parallel shifts in the dose-response curve. Schild regression analysis of the data established a pA2 value (6.46) similar to that reported for B1 receptor-mediated contraction. Although the relaxant effect of bradykinin was also inhibited by the B1 antagonist, parallel shifts in the dose response curve were not produced. Relaxation of the mesenteric artery by both des-Arg9-bradykinin and bradykinin was inhibited by the cyclooxygenase inhibitor indomethacin. The results of these studies indicate that in addition to vasoconstriction, des-Arg9-bradykinin can produce vasorelaxation which may be mediated through stimulation of B1 kinin receptors and the subsequent release of prostaglandins.

摘要

开展本研究以确定去精氨酸激肽是否能使离体血管舒张。去精氨酸9 -缓激肽和缓激肽均可使离体兔肠系膜上动脉产生剂量依赖性舒张。去精氨酸9 -缓激肽(ED50 = 7.2×10⁻⁹ M)的效力比缓激肽(ED50 = 6.1×10⁻⁸ M)强8.5倍。去精氨酸9 -缓激肽介导的舒张作用被特异性B1受体拮抗剂[亮氨酸8]去精氨酸9 -缓激肽抑制,该拮抗剂使剂量 - 反应曲线平行右移。对数据进行的Schild回归分析得出的pA2值(6.46)与报道的B1受体介导的收缩作用的pA2值相似。虽然缓激肽的舒张作用也被B1拮抗剂抑制,但未产生剂量反应曲线的平行右移。去精氨酸9 -缓激肽和缓激肽对肠系膜动脉的舒张作用均被环氧化酶抑制剂吲哚美辛抑制。这些研究结果表明,除血管收缩作用外,去精氨酸9 -缓激肽还可产生血管舒张作用,这可能是通过刺激B1激肽受体以及随后释放前列腺素介导的。

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