血管紧张素II,TRPV4 z-bo 2020-11-18 311

　　OBJECTIVE: By using transient receptor potential vanilloid type 4 (TRPV4) gene knockout (TRPV4-/ -) mice, to explore the role of TRPV4 receptor in angiotensin II (angiotensin II, Ang II). ) Role in induced kidney damage.

　　Methods: Experimental mice were divided into sham operation group and Ang II treatment group. Wild type and TRPV4-/-mice were subcutaneously perfused with Ang II to establish an Ang II dependent hypertension model, while sham operation group mice were perfused only subcutaneously Normal saline. After 4 weeks of treatment, the systolic blood pressure of the tail artery of the mice was measured. 24 h urine albumin excretion and 8-isomer prostaglandin. Changes in serum creatinine, and at the same time the pathological changes in kidney tissue...

　　Results: Compared with the corresponding sham operation group, the blood pressure of the mice in the Ang II treatment group increased? Urinary albumin and 8-isomeric prostaglandin excretion increased, accompanied by increased serum creatinine (P<0.05); renal small The degree of glomerular fibrosis and renal tubular interstitial injury were significantly aggravated, accompanied by an increase in the level of renal collagen (P <0.05). Except blood pressure, TRPV4 gene knockout can significantly inhibit all the pathological changes mentioned above, thereby alleviating the renal damage induced by Ang II (P <0.05).

　　Conclusion: In the process of AngII-induced hypertension, TRPV4 gene knockout can significantly attenuate the kidney damage induced by the above process. Therefore, the above research results suggest that TRPV4 receptor plays an important pathophysiological role in promoting Ang II-induced renal damage.