首页> 美国卫生研究院文献>Journal of the Renin-Angiotensin-Aldosterone System: JRAAS >Is angiotensin-(3–4) (Val-Tyr) the shortest angiotensin II-derived peptide opening new vistas on the renin–angiotensin system?
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Is angiotensin-(3–4) (Val-Tyr) the shortest angiotensin II-derived peptide opening new vistas on the renin–angiotensin system?

机译:血管紧张素II衍生的最短的血管紧张素-(3-4)(Val-Tyr)是否在肾素-血管紧张素系统上打开新的视野?

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摘要

Angiotensin-(3−4) (Ang-(3−4) or Val-Tyr) is the shorter angiotensin (Ang) II-derived peptide, formed through successive hydrolysis that culminates with the release of Val-Tyr as a dipeptide. It is formed both in plasma and in kidney from Ang II and Ang III, and can be considered a component of the systemic and organ-based renin–angiotensin system. It is potently antihypertensive in humans and rats, and its concerted actions on proximal tubule cells culminate in the inhibition of fluid reabsorption, hyperosmotic urinary excretion of Na+. At the renal cell signaling level, Ang-(3−4) counteracts Ang II-type 1 receptor-mediated responses by acting as an allosteric enhancer in Ang II-type 2 receptor populations that target adenosine triphosphate-dependent Ca2+ and Na+ transporters through a cyclic adenosine monophosphate-activated protein kinase pathway.
机译:血管紧张素(3-4)(Ang-(3-4)或Val-Tyr)是较短的血管紧张素(Ang)II衍生肽,通过连续水解形成,最终水解为二肽Val-Tyr。它由Ang II和Ang III在血浆和肾脏中形成,可以认为是系统性和基于器官的肾素-血管紧张素系统的组成部分。它在人和大鼠中均具有有效的降压作用,其对近端小管细胞的协同作用最终抑制了Na + 的液体重吸收,高渗尿液排泄。在肾细胞信号传导水平上,Ang-(3-4)通过充当靶向三磷酸腺苷依赖性Ca 2+的Ang II 2受体群中的变构增强剂,来抵消Ang II 1受体介导的反应。 和Na + 转运蛋白通过环状单磷酸腺苷激活的蛋白激酶途径。

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