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探索新领域：血管紧张素II、血管紧张素II 1型受体与远端曲小管中肾外髓质钾通道的相互作用

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

作者信息

Zhao Kun, Han Tiantian, Jia Linzhen, Wen Libo, Gao Renjun, Li Xue

机构信息

Basic Medical Science College, Qiqihar Medical University, Qiqihar, China.

Pharmacy College, Qiqihar Medical University, Qiqihar, China.

出版信息

Kidney Res Clin Pract. 2025 May;44(3):461-480. doi: 10.23876/j.krcp.24.023. Epub 2024 Sep 19.

DOI:10.23876/j.krcp.24.023
PMID:39384346
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12066336/
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.

摘要

背景

本研究调查了低钾摄入期间血管紧张素II（Ang II）对远曲小管（DCT）中肾外髓质钾通道（ROMK）活性的调节机制，重点关注由1型血管紧张素II受体（AT1R）介导的janus激酶2（JAK2）途径的激活。

方法

利用低钾饮食小鼠模型，采用膜片钳、逆转录定量聚合酶链反应、蛋白质免疫印迹和免疫组织化学染色等多种方法分析ROMK通道活性和相关蛋白的表达。

结果

研究结果表明，Ang II通过激活AT1R抑制DCT2膜中的ROMK活性，JAK2途径起核心作用。此外，抑制JAK2可逆转这种作用，表明其在高血压治疗中的潜力。

结论

本研究为Ang II在肾钾排泄和高血压病理生理学中的作用提供了新的见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eb79/12066336/d6f831baf89b/j-krcp-24-023f8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eb79/12066336/0a84f78d7c1a/j-krcp-24-023f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eb79/12066336/a30252960f91/j-krcp-24-023f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eb79/12066336/6890e1c3c4a4/j-krcp-24-023f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eb79/12066336/076b136ff4cb/j-krcp-24-023f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eb79/12066336/ca80938c70d6/j-krcp-24-023f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eb79/12066336/658972cb65d0/j-krcp-24-023f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eb79/12066336/1612fbb2e076/j-krcp-24-023f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eb79/12066336/d6f831baf89b/j-krcp-24-023f8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eb79/12066336/0a84f78d7c1a/j-krcp-24-023f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eb79/12066336/a30252960f91/j-krcp-24-023f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eb79/12066336/6890e1c3c4a4/j-krcp-24-023f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eb79/12066336/076b136ff4cb/j-krcp-24-023f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eb79/12066336/ca80938c70d6/j-krcp-24-023f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eb79/12066336/658972cb65d0/j-krcp-24-023f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eb79/12066336/1612fbb2e076/j-krcp-24-023f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eb79/12066336/d6f831baf89b/j-krcp-24-023f8.jpg

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Cardiovasc Res. 2023 Aug 7;119(9):1842-1855. doi: 10.1093/cvr/cvad086.
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Combination Therapy With Pulmonary Vasodilatation and JAK2 Inhibition for Pulmonary Hypertension With Polycythemia Vera.肺动脉扩张与JAK2抑制联合治疗真性红细胞增多症相关性肺动脉高压
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Interleukin-22 exacerbates angiotensin II-induced hypertensive renal injury.白细胞介素-22 加剧血管紧张素Ⅱ诱导的高血压性肾损伤。
Int Immunopharmacol. 2022 Aug;109:108840. doi: 10.1016/j.intimp.2022.108840. Epub 2022 May 11.
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