纹状体蛋白和caveolin-1(cav-1)是支架/调节蛋白,与盐敏感性高血压有关,并促进肾钠和水的重吸收,分别。盐皮质激素受体(MR)与striatin和cav-1相互作用,而醛固酮增加striatin和cav-1水平。然而,没有关于这些蛋白质在肾脏中水平的体内数据报道。
雄性Wistar大鼠腹腔注射生理盐水,仅醛固酮(Aldo:150μg/kg体重),或者用依普利酮预处理后的醛固酮,MR阻断剂,在醛固酮注射前30分钟(依普利酮[Ep。]+奥尔多)。注射醛固酮30分钟后,通过蛋白质印迹分析和免疫组织化学测定纹状体蛋白和cav-1的数量和定位,分别。
醛固酮使纹状体蛋白水平增加150%(P<0.05),cav-1水平下降200%(P<0.001)。依普利酮对纹状体素水平没有显著影响,但部分阻断了醛固酮诱导的cav-1水平升高。醛固酮刺激皮质和髓质的纹状体蛋白和cav-1免疫反应性。依普利酮降低了这两个区域的cav-1免疫染色;然而,皮层纹状体强度降低,但在髓质中增加。
这是第一个体内研究,证明醛固酮能迅速提高肾脏纹状体蛋白和cav-1的水平。醛固酮通过不依赖MR的途径增加纹状体素水平,而cav-1部分通过MR调节。
Striatin and caveolin-1 (cav-1) are scaffolding/regulating proteins that are associated with salt-sensitive high blood pressure and promote renal sodium and water reabsorption, respectively. The mineralocorticoid receptor (MR) interacts with
striatin and cav-1, while aldosterone increases
striatin and cav-1 levels. However, no in vivo data have been reported for the levels of these proteins in the kidney.
Male Wistar rats were intraperitoneally injected with normal saline solution, aldosterone alone (Aldo: 150 μg/kg body weight), or aldosterone after pretreatment with eplerenone, an MR blocker, 30 minutes before the aldosterone injection (eplerenone [Ep.]+Aldo). Thirty minutes after the aldosterone injection, the amount and localization of
striatin and cav-1 were determined by Western blot analysis and immunohistochemistry, respectively.
Aldosterone increased
striatin levels by 150% (P<0.05), and cav-1 levels by 200% (P<0.001). Eplerenone had no significant effect on striatin levels, but partially blocked the aldosterone-induced increase in cav-1 levels. Aldosterone stimulated
striatin and cav-1 immunoreactivity in both the cortex and medulla. Eplerenone reduced cav-1 immunostaining in both areas; however, striatin intensity was reduced in the cortex, but increased in the medulla.
This is the first in vivo study demonstrating that aldosterone rapidly enhances renal levels of striatin and cav-1. Aldosterone increases striatin levels via an MR-independent pathway, whereas cav-1 is partially regulated through MR.