• 首页期刊简介编委会刊物订阅专栏专刊电子刊学术动态联系我们English
引用本文:孙洞箫,周盾,邱振宇.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[J].中国现代应用药学,2010,27(10):857-860.
.Effect of Angiotensin II on Intracellular Free Calcium Concentration in RASMCs and Antagonism of Losartan[J].Chin J Mod Appl Pharm(中国现代应用药学),2010,27(10):857-860.
【打印本页】   【HTML】   【下载PDF全文】   查看/发表评论  【EndNote】   【RefMan】   【BibTex】
←前一篇|后一篇→ 过刊浏览    高级检索
本文已被:浏览 1995次   下载 2106 本文二维码信息
码上扫一扫!
分享到: 微信 更多
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
孙洞箫,周盾,邱振宇
作者单位
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。
关键词:  肾小球入球小动脉细胞  高血压  血管紧张素Ⅱ  Losartan  细胞内钙离子浓度
DOI:
分类号:
基金项目:
Effect of Angiotensin II on Intracellular Free Calcium Concentration in RASMCs and Antagonism of Losartan
SUN Dongxiao  ZHOU Dun  QIU Zhenyu
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.

Key words:  RASMCs  hypertension  angiotensinⅡ  Losartan  intracellular free calcium concentration
扫一扫关注本刊微信