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

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（Ca^2＋]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0.1μmol.L^-1AngⅡ;Losartan组：加入终浓度为50μmol.L^-1Losartan;AngⅡ＋Losartan组：同时加入Losartan 50μmol.L^-1AngⅡ0.1μmol.L^-1负载后上机检测Ca^2＋]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Ca^2＋]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Ca^2＋]i的上升,导致细胞收缩,因此Ca^2＋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Ca^2＋超载。

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

OBJECTIVE To explore the effects of angiotensin（Ang Ⅱ） on intracellular free calcium concentration（Ca^2＋]i） in RASMCs and antagonism of Losartan.METHODS RASMCs were isolated and divided into four groups： control group,Ang Ⅱ group,Losartan group and Ang Ⅱ ＋Losartan group.Confocal microscope was used with Fluo-3/AM as an indicator to detect the changes of Ca^2＋]i.RESULTS Compared with control group,intracellular fluorescent intensity of RASMCs had no change in Losartan group,and was significantly higher in Ang Ⅱ group（P〈0.05）.Value in Ang Ⅱ ＋Losartan group was significantly lower than that in Ang Ⅱ group（P〈0.05）.CONCLUSION Ang Ⅱ may induce intracellular calcium overload in RASMCs,which can be significantly reduced by Losartan.