Suppr超能文献

介导内皮素-1或IRL 1620在豚鼠离体气道中引起收缩的ETB受体的特性:BQ-123、FR139317或PD 145065的作用

Characterization of ETB receptors mediating contractions induced by endothelin-1 or IRL 1620 in guinea-pig isolated airways: effects of BQ-123, FR139317 or PD 145065.

作者信息

Battistini B, Warner T D, Fournier A, Vane J R

机构信息

William Harvey Research Institute, St. Bartholomew's Hospital Medical College, London.

出版信息

Br J Pharmacol. 1994 Apr;111(4):1009-16. doi: 10.1111/j.1476-5381.1994.tb14844.x.

Abstract
  1. We have characterized the receptors mediating contractions to endothelin-1 (ET-1) or IRL 1620, an ETB receptor selective agonist, in isolated strips of tissue prepared from different parts of the guinea-pig airways. We used as antagonists BQ-123 and FR139317 (ETA receptor-selective) and PD 145065 (ETA/ETB receptor non-selective). 2. ET-1 and IRL 1620 (10(-10) M to 10(-6) M) caused similar concentration-dependent contractions of strips of guinea-pig trachea and upper bronchus. In the guinea-pig trachea without epithelium or lung parenchyma, IRL 1620 was less potent than ET-1. 3. In the trachea, contraction to ET-1 (< 10(-8) M) was preceded by a transient relaxation which was inhibited by BQ-123 (10(-5) M) or FR 139317 (10(-5) M) or by the removal of the epithelium. The concentration-response curve to ET-1 in the trachea was shifted to the right by PD 145065 (10(-5) M to 10(-4) M). PD 145065 (10(-4) M) also inhibited the response to ET-1 (3 x 10(-7) M) by 55%. Contractions induced by IRL 1620 were not affected by BQ-123 (10(-6) M) or FR139317 (10(-6) M) but were significantly attenuated by 10(-5) M of either antagonist. PD 145065 at 10(-6) M strongly attenuated and at 10(-5) M abolished contractions induced by IRL 1620. 4. In the trachea, removal of the epithelium potentiated the effects of both agonists. BQ-123 (10-5 M)had no effect on contractions of the trachea without epithelium induced by ET-1, but FR139317 (10-5 M)caused a significant inhibition. PD 145065 (10-5 M to 10-4 M) caused a shift to the right of the ET-1 concentration-response curve without affecting the contractile effect at 3 x 10-7 M. All three antagonists inhibited contractions induced by IRL 1620.5. In the upper bronchus, BQ-123 (10-5 M) did not affect contractions induced by ET-1, whileFR139317 (10-5 M) attenuated (20-26%) only contractions induced by 1-3 x 10-7 M ET-1. PD 145065(10-5 M to 10-4 M) caused a shift to the right of the ET-1 concentration-response curve. The contractions induced by IRL 1620 were inhibited by BQ-123 or FR139317 (10-5M to 10-4 M). PD 145065(10-6 M) strongly inhibited contractions induced by IRL 1620 and PD 145065 (10-5 M) totally abolished them.6. The contractile action of ET-1 in the lung parenchyma was significantly and similarly attenuated by BQ-123 (10-5 M) or indomethacin (10-5 M), while FRI39317 (10-5 M) was less effective. PD 145065(10-6 to 10-5 M) inhibited contractions to ET-1. IRL 1620, which is less potent than ET-1 in this preparation, was antagonized by PD 145065 (10-5 to 10-6 M) but unaffected by BQ-123 (10-6 M to10-5M) or FR139317 (10-6 M).7. Thus, ETB receptors mediate contractions to ET-1 in all four guinea-pig airway preparations. In addition, contractions to ET-1 in the trachea and lung parenchyma are mediated in part by ETA receptors. In the latter tissue, these ETA receptors mediate contraction through the release of cyclooxygenase metabolites. Similarly, ETA receptors located on the epithelial cells also mediate the release of prostanoids in the trachea with epithelium but they are responsible for transient relaxations. Interestingly,contractions induced by IRL 1620 were more susceptible to inhibition by the different antagonists,most probably because it binds to the endothelin receptors in a reversible manner. High concentrations(10-5 M) of ETA-selective antagonists also inhibit responses to IRL 1620, most probably by an effect at ETB receptors in both the trachea and the upper bronchus.
摘要
  1. 我们已对介导豚鼠气道不同部位制备的离体组织条对内皮素 -1(ET -1)或IRL 1620(一种ETB受体选择性激动剂)产生收缩反应的受体进行了表征。我们使用BQ -123和FR139317(ETA受体选择性拮抗剂)以及PD 145065(ETA/ETB受体非选择性拮抗剂)作为拮抗剂。2. ET -1和IRL 1620(10⁻¹⁰ M至10⁻⁶ M)引起豚鼠气管和上支气管条类似的浓度依赖性收缩。在无上皮或肺实质的豚鼠气管中,IRL 1620的效力低于ET -1。3. 在气管中,ET -1(<10⁻⁸ M)引起的收缩之前有短暂的舒张,这被BQ -123(10⁻⁵ M)或FR 139317(10⁻⁵ M)或去除上皮所抑制。气管中ET -1的浓度 - 反应曲线被PD 145065(10⁻⁵ M至10⁻⁴ M)向右移动。PD 145065(10⁻⁴ M)也使对ET -1(3×10⁻⁷ M)的反应抑制了55%。IRL 1620诱导的收缩不受BQ -123(10⁻⁶ M)或FR139317(10⁻⁶ M)影响,但被10⁻⁵ M的任何一种拮抗剂显著减弱。10⁻⁶ M的PD 145065强烈减弱并在10⁻⁵ M时消除IRL 1620诱导的收缩。4. 在气管中,去除上皮增强了两种激动剂的作用。BQ -123(10⁻⁵ M)对ET -1诱导的无上皮气管收缩无影响,但FR139317(10⁻⁵ M)引起显著抑制。PD 145065(10⁻⁵ M至10⁻⁴ M)使ET -1浓度 - 反应曲线向右移动,而不影响3×10⁻⁷ M时的收缩效应。所有三种拮抗剂均抑制IRL 1620诱导的收缩。5. 在上支气管中,BQ -123(10⁻⁵ M)不影响ET -1诱导的收缩,而FR139317(10⁻⁵ M)仅减弱(20 - 26%)1 - 3×10⁻⁷ M ET -1诱导的收缩。PD 145065(10⁻⁵ M至10⁻⁴ M)使ET -1浓度 - 反应曲线向右移动。IRL 1620诱导的收缩被BQ -123或FR139317(10⁻⁵ M至10⁻⁴ M)抑制。PD 145065(10⁻⁶ M)强烈抑制IRL 1620诱导的收缩,而PD 145065(10⁻⁵ M)完全消除它们。6. ET -1在肺实质中的收缩作用被BQ -123(10⁻⁵ M)或吲哚美辛(10⁻⁵ M)显著且类似地减弱,而FRI39317(10⁻⁵ M)效果较差。PD 145065(10⁻⁶至10⁻⁵ M)抑制对ET -1的收缩。在该制剂中效力低于ET -1的IRL 1620被PD 145065(10⁻⁵至10⁻⁶ M)拮抗,但不受BQ -123(10⁻⁶ M至10⁻⁵ M)或FR139317(10⁻⁶ M)影响。7. 因此,ETB受体介导豚鼠气道所有四个制剂中对ET -1的收缩反应。此外,气管和肺实质中对ET -1的收缩部分由ETA受体介导。在后者组织中,这些ETA受体通过环氧化酶代谢产物的释放介导收缩。同样,位于上皮细胞上的ETA受体也介导有上皮气管中前列腺素的释放,但它们负责短暂的舒张。有趣的是,IRL 1620诱导的收缩更容易被不同拮抗剂抑制,很可能是因为它以可逆方式与内皮素受体结合。高浓度(10⁻⁵ M)的ETA选择性拮抗剂也抑制对IRL 1620的反应,很可能是通过对气管和上支气管中ETB受体的作用。

相似文献

3
Endothelin receptor subtypes in human and guinea-pig pulmonary tissues.人和豚鼠肺组织中的内皮素受体亚型
Br J Pharmacol. 1993 Nov;110(3):1175-83. doi: 10.1111/j.1476-5381.1993.tb13938.x.

引用本文的文献

1
Airway epithelial compression promotes airway smooth muscle proliferation and contraction.气道上皮压缩促进气道平滑肌增殖和收缩。
Am J Physiol Lung Cell Mol Physiol. 2018 Nov 1;315(5):L645-L652. doi: 10.1152/ajplung.00261.2018. Epub 2018 Aug 2.
2
Endothelin and hepatic wound healing.内皮素与肝损伤修复。
Pharmacol Res. 2011 Jun;63(6):512-8. doi: 10.1016/j.phrs.2011.03.005. Epub 2011 Mar 21.

本文引用的文献

6
Endothelin and the respiratory system.内皮素与呼吸系统。
Trends Pharmacol Sci. 1993 Jan;14(1):29-32. doi: 10.1016/0165-6147(93)90111-v.

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验