高级检索

    血管紧张素Ⅱ对大鼠肾入球小动脉细胞内钙离子浓度的影响及Losartan的拮抗作用

    Effect of Angiotensin II on Intracellular Free Calcium Concentration in RASMCs and Antagonism of Losartan

      摘要
    • 摘要: 目的 探讨血管紧张素Ⅱ(AngⅡ)对肾小球入球小动脉细胞内钙离子浓度(Ca2+i)的影响与高血压肾小动脉重建的关系及Losartan的治疗作用。方法 细胞培养：大鼠肾小球入球小动脉细胞随机分为4组。对照组：不加AngⅡ处理；AngⅡ组：加入终浓度为0.1 μmol·L-1的AngⅡ；Losartan组：加入终浓度为50 μmol·L-1的Losartan；AngⅡ+Losartan组：同时加入Losartan 50 μmol·L-1和AngⅡ0.1 μmol·L-1。负载后上机检测Ca2+i。结果 细胞培养显示AngⅡ引起了细胞收缩变化，表现为胞突变细变短，胞突回缩，胞体变圆，细胞长度与直径均明显缩小。Losartan处理组较AngⅡ组细胞形态变化减轻且Losartan对AngⅡ增高RASMCs内Ca2+i有明显抑制作用。结论 AngⅡ可引起肾小球入球小动脉细胞内Ca2+i的上升，导致细胞收缩，因此Ca2+超载可能是肾素-血管紧张素系统起作用的重要环节。Losartan可抑制细胞内Ca2+超载。

       

      Abstract: OBJECTIVE To explore the effects of angiotensin(Ang Ⅱ) on intracellular free calcium concentration(Ca2+i) in RASMCs and antagonism of Losartan. METHODS RASMCs were isolated and divided into four groups: control group, AngⅡ group, Losartan group and Ang Ⅱ+Losartan group. Confocal microscope was used with Fluo-3/AM as an indicator to detect the changes of Ca2+i. RESULTS Compared with control group, intracellular fluorescent intensity of RASMCs had no change in Losartan group, and was significantly higher in AngⅡ group (P<0.05). Value in AngⅡ+Losartan group was significantly lower than that in AngⅡ group (P<0.05). CONCLUSION AngⅡ may induce intracellular calcium overload in RASMCs, which can be significantly reduced by Losartan.

       

      • HTML全文
      • 参考文献(8)
      • 相关文章
      • 施引文献
    • 资源附件(0)

    /

    返回文章
    返回