Exploring new horizons: angiotensin II, angiotensin II type 1 receptor, and renal outer medullary potassium channel interaction in distal convoluted tubule.

IF 2.9 3区 医学 Q1 UROLOGY & NEPHROLOGY
Kun Zhao, Tiantian Han, Linzhen Jia, Libo Wen, Renjun Gao, Xue Li
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引用次数: 0

Abstract

Background: This study investigates angiotensin II (Ang II)'s regulatory mechanism on renal outer medullary potassium channel (ROMK) activity in the distal convoluted tubule (DCT) during low potassium intake, focusing on the Janus kinase 2 (JAK2) pathway activation mediated by the Ang II type 1 receptor (AT1R).

Methods: Utilizing a low potassium diet mouse model, various methods including patch clamping, reverse transcription-quantitative polymerase chain reaction, Western blotting, and immunohistochemical staining were applied to analyze ROMK channel activity and the expression of related proteins.

Results: The findings reveal that Ang II inhibits ROMK activity in the DCT2 membrane through AT1R activation, with the JAK2 pathway playing a central role. Further, inhibiting JAK2 reverses this effect, indicating its potential in hypertension treatment.

Conclusion: This study provides novel insights into the role of Ang II in renal potassium excretion and hypertension pathophysiology.

探索新视野:远曲小管中血管紧张素 II、血管紧张素 II 1 型受体和肾外髓钾通道的相互作用。
背景:本研究探讨了低钾摄入时血管紧张素II(Ang II)对远曲小管(DCT)肾外髓质钾通道(ROMK)活性的调控机制,重点研究了Ang II 1型受体(AT1R)介导的Janus激酶2(JAK2)通路激活:方法:利用低钾饮食小鼠模型,采用贴片钳夹、逆转录-定量聚合酶链反应、Western印迹和免疫组化染色等多种方法分析ROMK通道活性及相关蛋白的表达:结果:研究结果表明,Ang II通过激活AT1R抑制DCT2膜中ROMK的活性,其中JAK2通路起着核心作用。此外,抑制 JAK2 能逆转这种效应,表明其在高血压治疗中的潜力:这项研究为了解 Ang II 在肾脏钾排泄和高血压病理生理学中的作用提供了新的视角。
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来源期刊
CiteScore
4.60
自引率
10.00%
发文量
77
审稿时长
10 weeks
期刊介绍: Kidney Research and Clinical Practice (formerly The Korean Journal of Nephrology; ISSN 1975-9460, launched in 1982), the official journal of the Korean Society of Nephrology, is an international, peer-reviewed journal published in English. Its ISO abbreviation is Kidney Res Clin Pract. To provide an efficient venue for dissemination of knowledge and discussion of topics related to basic renal science and clinical practice, the journal offers open access (free submission and free access) and considers articles on all aspects of clinical nephrology and hypertension as well as related molecular genetics, anatomy, pathology, physiology, pharmacology, and immunology. In particular, the journal focuses on translational renal research that helps bridging laboratory discovery with the diagnosis and treatment of human kidney disease. Topics covered include basic science with possible clinical applicability and papers on the pathophysiological basis of disease processes of the kidney. Original researches from areas of intervention nephrology or dialysis access are also welcomed. Major article types considered for publication include original research and reviews on current topics of interest. Accepted manuscripts are granted free online open-access immediately after publication, which permits its users to read, download, copy, distribute, print, search, or link to the full texts of its articles to facilitate access to a broad readership. Circulation number of print copies is 1,600.
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