Suppr超能文献

多种血管紧张素受体类型是否参与血管紧张素(1-7)对离体大鼠门静脉的作用?

Are multiple angiotensin receptor types involved in angiotensin (1-7) actions on isolated rat portal vein.

作者信息

Gurzu Bogdan, Costuleanu Marcel, Slatineanu Simona Mihaela, Ciobanu Aurica, Petrescu Gheorghe

机构信息

Department of Physiology, Faculty of Dentistry, University of Medicine and Pharmacy "Gr. T. Popa", Iasi, RO-700115, Romania.

出版信息

J Renin Angiotensin Aldosterone Syst. 2005 Sep;6(2):90-5. doi: 10.3317/jraas.2005.015.

Abstract

Angiotensin (1-7) [Ang (1-7)] is a bioactive component of the renin angiotensin system. Ang (1-7) may interact with angiotensin type 1 (AT1) or type 2 (AT2) receptors and with Ang (1-7) - specific receptors. We examined the interactions between different doses of Ang (1-7) (1 nM-1 microM) and angiotensin II (Ang II) (10 and 100 nM) on isolated rat portal vein. In endothelium-denuded portal vein rings, Ang (1-7) inhibited contractile effects induced by Ang II. The effects of Ang (1-7) were modified by indomethacin, N(G)-nitro-L-arginine methyl ester (L-NAME), (D-Ala7)-Angiotensin (1-7) (H-2888) and losartan. Our results suggest that on rat isolated portal vein rings without endothelium, Ang (1-7) reduces Ang II-induced contractions by acting mostly on Ang (1-7) specific receptors, and this effect is mediated by vasodilatatory prostaglandins. At high concentrations, Ang (1-7) effects are mediated by AT1-receptors, though to a lesser extent than by Ang (1-7) specific receptors.

摘要

血管紧张素(1-7)[Ang(1-7)]是肾素血管紧张素系统的一种生物活性成分。Ang(1-7)可能与1型血管紧张素(AT1)或2型血管紧张素(AT2)受体以及Ang(1-7)特异性受体相互作用。我们研究了不同剂量的Ang(1-7)(1 nM - 1 μM)与血管紧张素II(Ang II)(10和100 nM)对离体大鼠门静脉的相互作用。在内皮剥脱的门静脉环中,Ang(1-7)抑制了Ang II诱导的收缩效应。Ang(1-7)的作用受到吲哚美辛、N(G)-硝基-L-精氨酸甲酯(L-NAME)、(D-Ala7)-血管紧张素(1-7)(H-2888)和氯沙坦的影响。我们的结果表明,在无内皮的大鼠离体门静脉环上,Ang(1-7)主要通过作用于Ang(1-7)特异性受体来减少Ang II诱导的收缩,且这种作用由血管舒张性前列腺素介导。在高浓度时,Ang(1-7)的作用由AT1受体介导,尽管程度低于Ang(1-7)特异性受体。

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