TRPC1通道参与调节肾小球系膜细胞的收缩

Involvement of canonical transient receptor potential 1 channel in the contractile function of glomerular mesangial cells

目的探讨离体和在体情况下TRPC1通道是否参与肾小球系膜细胞的收缩。方法通过计算细胞表面积来观察肾小球系膜细胞的收缩情况。分别利用荧光标记的菊粉和对氨基马尿酸（PAH）的血浆清除率计算大鼠肾小球滤过率（GFR）和肾血浆流量。结果在肾小球系膜细胞的培养液中加入血管紧张素Ⅱ（AngⅡ）10min后，细胞表面积减少（37．2％±4．0％），系膜细胞的收缩反应可因TRPC1基因敲除而受到显著抑制（20．1％±3．0％）。给大鼠注射AngⅡ（1．7ng·min^-1·100g^-1BW）可引起GFR下降，注射TRPC1抗体（300μg／L）显著抑制AngⅡ引起GFR下降（P〈0．05）。但与TRPC1抗体相同浓度的免疫球蛋白，不能抑制AngⅡ引起的GFR下降。另外，TRPC1抗体不影响AngⅡ引起的血压改变和肾血流量的下降。结论本实验表明TRPC1通道在调节肾小球系膜细胞收缩功能方面发挥了重要的作用。

Objective To investigate whether canonical transient receptor potential 1 （TRPC1） channel took part in masangial cell （MC） contraction. Methods The Ang Ⅱ-induced contraction on MCs was measured by changes in planar surface area. Glomerular filtration rate （GFR） and renal blood flow were estimated by measurement of FITC-inulin and para-aminohippurate （PAH） plasma clearances, respectively. Results After treatment with Ang Ⅱ for 10 min, the surface area of the control MCs was decreased by （37.2 ± 4. 0） %. However, the contractile responses of the MCs with TRPC1 knockdown were significantly attenuated [（20. 1 ± 3.0）%]. In intact rats, systemic infusion of Ang Ⅱ （1.7 ng·min^-1·100 g^-1 BW） caused a decrease in GFR. The Ang Ⅱ-induced GFR decrease was significantly inhibited by infusion of TRPC1 antibody （300 μg/L） （P〈0. 05）, but not by the same concentration of its immunoglobulin. However, the treatment of TRPC1 antibody did not affect the effect of the vasopressure and renal blood flow caused by Ang Ⅱ. Conclusion TRPC1 channel plays an important role in MC contraction.