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Direct activation of ENaC by angiotensin II: Recent advances and new insights

机译:血管紧张素II直接激活ENaC:最新进展和新见解

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Angiotensin II (Ang II) is the principal effector of the renin-angiotensin-aldosterone system (RAAS). It initiates myriad processes in multiple organs integrated to increase circulating volume and elevate systemic blood pressure. In the kidney, Ang II stimulates renal tubular water and salt reabsorption causing antinatriuresis and antidiuresis. Activation of the RAAS is known to enhance activity of the epithelial Na+ channel (ENaC) in the aldosterone-sensitive distal nephron. In addition to its well described stimulatory actions on aldosterone secretion, Ang II is also capable of directly increasing ENaC activity. In this brief review, we discuss recent findings about non-classical Ang II actions on ENaC and speculate about its relevance for renal sodium handling.
机译:血管紧张素II(Ang II)是肾素-血管紧张素-醛固酮系统(RAAS)的主要效应物。它在整合的多个器官中引发无数过程,以增加循环量并升高全身性血压。在肾脏中,Ang II刺激肾小管水和盐分的重吸收,从而导致排尿利尿和抗利尿作用。已知RAAS的激活可增强醛固酮敏感的远端肾单位中上皮Na +通道(ENaC)的活性。除了对醛固酮分泌的良好刺激作用外,Ang II还能够直接增加ENaC活性。在这篇简短的综述中,我们讨论了有关非经典Ang II对ENaC的作用的最新发现,并推测了其与肾钠处理的相关性。

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