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.

Renal interstitial fibrosis（RIF） is the main pathological manifestation of chronic kidney disease. Due to the complexity of the mechanism， there is no specific treatment for RIF in clinical practice. The abnormal activation of the phosphatidylinositol 3-kinase （PI3K）/protein kinase B（Akt） signaling pathway and the activation of downstream target genes are key drivers of RIF induction and progression. Traditional Chinese medicine has the characteristics of precise efficacy and minimal toxic side effects， and the occurrence and development of RIF can be regulated by multiple targets and mutual coordination. This review focuses on the PI3K/Akt signaling pathway and summarizes the potential targets and regulatory mechanisms of traditional Chinese medicine in the treatment of RIF. It is found that various effective ingredients （such as sinomenine， mangiferin， coumarin derivates from Hydrangea paniculata， etc.） and formulas （such as Fushengong decoction， Qi-Bang-Yi-Shen formula， etc.） of traditional Chinese medicine can inhibit fibroblast proliferation， improve inflammation and oxidative stress， maintain mitochondrial stability， and slow down ferroptosis through this pathway， thereby delaying the occurrence and progression of RIF.