TRPV4 contributes to renal injury induced by angiotensin II in mice

To determine whether deletion of TRPV4 attenuates angiotensin II (Ang II)‐induced renal injury, Ang II was infused systemically into wild type (WT) and TRPV4‐null mutant (TRPV4 ‐/‐ ) mice for 4 weeks. Systolic blood pressure increased in Ang II‐treated WT or TRPV4 ‐/‐ mice with the similar degree (P>0.05). Ang II treatment increased urinary excretion of albumin and 8‐isoprostane, and decreased creatinine clearance in both WT and TRPV4 ‐/‐ mice with a greater magnitude in the former strain (P<0.05). Periodic acid‐Schiff and Masson's trichrome staining showed that kidneys of Ang II‐treated WT mice exhibited more severe glomerulosclerosis and tubulointerstitial injury compared with Ang II‐treated TRPV4 ‐/‐ mice (P<0.05). Hydroxyproline assay and F4/80‐staining showed that renal collagen levels and monocyte/macrophage infiltration were greater in Ang II‐treated WT mice compared with TRPV4 ‐/‐ mice (P<0.05). Thus, our data show that deletion of TRPV4 alleviates renal injury in the absence of alteration in blood pressure in Ang II‐hypertensive mice, indicating that TRPV4 could serve as a novel target for treating renal injury associated with hypertension. [This work was supported by grants from the National Natural Science Foundation of China (No.81170243) and Henan Provincial Science and Technology Innovative Program for Outstanding Scholarship (No. 124200510007)].