异氟醚可能通过ERK磷酸化增强肾动脉平滑肌收缩  

Isoflurane increase renal artial smooth muscle contraction may through phosphorylated ERK1/2 pathway

作　　者：汉建忠[1] 罗自强[1] 

机构地区：[1]中南大学基础医学院生理学系,湖南长沙410078

出　　处：《中国药理学通报》2005年第3期332-335,共4页Chinese Pharmacological Bulletin

摘　　要：目的实验观察异氟醚对去内皮肾动脉血管平滑肌收缩增强的作用,并观察肾动脉血管平滑肌细胞在异氟醚的作用下细胞内MAPK通路的激活状态,以探讨异氟醚引发肾动脉血管平滑肌收缩增强的可能信号通路。方法①去内皮肾动脉条,3%皂苷处理使膜通透,咖啡因诱除内质网内贮钙,利用10-6钙离子浓度EGTA缓冲液平衡后,应用接近最大的钙离子浓度的EGTA缓冲液使肾动脉条压缩达平衡,加入不同浓度异氟醚EGTA缓冲溶液,观察动脉条张力变化。②1%、3%、5%异氟醚分别作用于培养的肾动脉血管平滑肌细胞,提取细胞内蛋白,Westenblot检测ERK磷酸化的变化。结果异氟醚能使压缩达平衡的肾动脉环张力进一步增强,且与异氟醚浓度呈剂量依赖性。随异氟醚浓度的增加,培养的肾动脉血管平滑肌细胞内ERK1/2(p44/42)磷酸化逐步增强,并随时间增强,在15min后,逐渐下降。Aim This study was to investigate the effect of isoflurane on contracted renal arterial smooth muscle and to determine whether the MAPK pathway is involved in the intracellular signaling. Methods ①Rabbit renal arterial strips were treated with sapoin to make the sarcolemma permeability. And the calcium stored in reticulum (SR) was released using caffeine.Stead state tense was obtained when the strips were soaked in submaximal calcium concentration buffer.Then the submaximal calcium concentration buffer with various concentration isoflurane was admininstered,the change of tensions was detected.②primary renal arterial smooth muscle cells were cultured and treated with different concentration of isoflurane for different duration,and the levels of phosphorylated ERK1/2 in different groups were detected with western blot.Result Isoflurane all caused rabbit renal artery strips further contraction after they have reached equilibrium,and the tension altitude was isoflurane concentration dependent. Isoflurane upregulates ERK1/2 (p44/42) phosphorylation in cultured renal arterial smooth muscle cells in a concentration and time depend way.Conclusion Isoflurane can upregulates the tension of contracted renal arterial smooth muscle. And it may involve the activation of p44/42 MAPK pathway.

关 键 词：异氟醚 肾动脉 血管平滑肌 ERK 1/2 

分 类 号：R-332[医药卫生] R322.121