Relaxation of isolated mesenteric arteries by des-Arg9-bradykinin stimulation of B1 receptors.
Relaxation of isolated mesenteric arteries by des-Arg9-bradykinin stimulation of B1 receptors.
复制标题
通过 des-Arg9-缓激肽刺激 B1 受体来舒张孤立的肠系膜动脉。
DOI：
10.1016/0014-2999(86)90178-0
复制
发表时间：
1986
影响因子：
5
通讯作者：
Ward,PE
中科院分区：
文献类型：
--
作者：
Churchill,L;Ward,PE
目前的研究进行，以确定是否des-Arg-激肽可以产生离体血管舒张。des-Arg 9-缓激肽和缓激肽都产生了剂量依赖性的松弛离体兔肠系膜上级动脉。Des-Arg 9-缓激肽（ED 50 = 7.2 × 10− 9 M）的效力是缓激肽（ED 50 = 6.1 × 10− 8 M）的8.5倍。特异性B1受体拮抗剂[Leu 8] des-Arg 9-缓激肽可抑制Des-Arg 9-缓激肽介导的舒张作用，并使剂量-反应曲线平行移动。Schild回归分析的数据建立了一个pA 2值（6.46）类似于B1受体介导的收缩报告。虽然缓激肽的舒张作用也被B1受体拮抗剂抑制，但剂量反应曲线没有平行移动。脱精氨酸缓激肽和缓激肽对肠系膜动脉的舒张作用可被环加氧酶抑制剂吲哚美辛抑制。这些研究的结果表明，除了血管收缩，脱精氨酸缓激肽可以产生血管舒张，这可能是通过刺激B1激肽受体和随后释放的肾上腺素介导的。
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 × 10−9M) was 8.5 times more potent than bradykinin (ED50= 6.1 × 10−8M). Des-Arg9-bradykinin-mediated relaxation was inhibited by the specific B1receptor antagonist [Leu8]des-Arg9-bradykinin which produced parallel shifts in the dose-response curve. Schild regression analysis of the data established a pA2value (6.46) similar to that reported for B1receptor-mediated contraction. Although the relaxant effect of bradykinin was also inhibited by the B1antagonist, 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 B1kinin receptors and the subsequent release of prostaglandins.