Isoflurane alters angiotensin II-induced Ca2+ mobilization in aortic smooth muscle cells from hypertensive rats: implication of cytoskeleton.
Isoflurane alters angiotensin II-induced Ca2+ mobilization in aortic smooth muscle cells from hypertensive rats: implication of cytoskeleton.
复制标题
异氟烷改变高血压大鼠主动脉平滑肌细胞中血管紧张素 II 诱导的 Ca2+ 动员：细胞骨架的意义。
DOI：
10.1097/00000542-200209000-00019
复制
发表时间：
2002
期刊：
影响因子：
8.8
通讯作者：
G. Dagher
中科院分区：
文献类型：
--
作者：
E. Samain;H. Bouillier;C. Rucker;J. Mazoit;J. Marty;J. Renaud;G. Dagher
背景
血管紧张素II（AngII）是一种有效的血管收缩剂，参与动脉血压的短期控制。据报道，异氟烷通过改变血管平滑肌细胞对几种激动剂的血管紧张性反应来降低血管张力，但其对AngII信号传导的影响尚不清楚。另一方面，血管对AngII的反应在高血压中改变。在本研究中，作者检验了以下假设：（1）异氟烷改变了Wistar京都大鼠和自发性高血压大鼠主动脉血管平滑肌细胞中AngII诱导的细胞内Ca动员，（2）该效应可能与微管网络组织的改变相关，据报告，微管网络组织参与AngII信号传导。
方法
研究了0.5-3%异氟醚的作用：（1）使用荧光成像显微镜，在分离自6周龄Wistar京都和自发性高血压大鼠的负载Fura-2的培养的主动脉血管平滑肌细胞中，对AngII（10 μ m）诱导的细胞内Ca动员、细胞内Ca从内部储存释放和Ca内流的影响;和（2）对组织的细胞骨架元素，使用免疫荧光标记。
结果
在这两种染色剂中，异氟烷以浓度依赖性方式降低AngII诱导的细胞内Ca动员、内部储存的Ca释放和通过硝苯地平不敏感的Ca通道的Ca内流。这种效应发生在Wistar京都大鼠中异氟烷浓度低于自发性高血压大鼠中。在这两种菌株中，异氟烷对AngII-Ca动员的影响被诺考达唑、长春碱或紫杉醇对微管聚合的损害所消除。异氟烷以浓度依赖性和可逆的方式直接改变肾小管网络组织。
结论
在临床相关浓度下，异氟烷可降低AngII诱导的Ca动员，表明血管对AngII的反应可在异氟烷麻醉期间改变。发现高血压应变的敏感性低于正常血压应变。在这两种菌株中，异氟烷效应与微管网络相互作用相关。
BACKGROUND
Angiotensin II (AngII) is a potent vasoconstrictor involved in the short-term control of arterial blood pressure. Isoflurane was reported to decrease vascular tone through an alteration of vascular smooth muscle cell vasomotor response to several agonists, but its effect on AngII signaling is not known. On the other hand, vascular response to AngII is altered in hypertension. In this study, the authors tested the hypothesis that (1) isoflurane alters AngII-induced intracellular Ca mobilization in aortic vascular smooth muscle cell from Wistar Kyoto and spontaneously hypertensive rats, and (2) this effect could be associated with an alteration of the organization of microtubular network, reported to be involved in AngII signaling.
METHODS
The effect of 0.5-3% isoflurane was studied (1) on AngII (10 m)-induced intracellular Ca mobilization, intracellular Ca release from internal stores, and Ca influx in Fura-2 loaded cultured aortic vascular smooth muscle cell isolated from 6-week-old Wistar Kyoto and spontaneously hypertensive rats, using fluorescent imaging microscopy; and (2) on the organization of cytoskeletal elements, using immunofluorescence labeling.
RESULTS
In both stains, isoflurane decreased in a concentration-dependent manner AngII-induced intracellular Ca mobilization, Ca release from internal stores, and Ca influx through nifedipine-insensitive Ca channels. This effect occurred at a lower concentrations of isoflurane in Wistar Kyoto rats than in spontaneously hypertensive rats. In both strains, the effect of isoflurane on AngII- Ca mobilization was abolished by impairment with nocodazole, vinblastine, or paclitaxel of microtubules polymerization. Isoflurane directly altered tubular network organization in a concentration-dependent and reversible manner.
CONCLUSIONS
Isoflurane decreased AngII-induced Ca mobilization at clinically relevant concentrations, suggesting that vascular response to AngII could be altered during isoflurane anesthesia. The hypertensive strain was found less sensitive than the normotensive one. In both strains, the isoflurane effect was associated with a microtubular network interaction.
影响因子：
4
作者：
E. Moore;P. L. Becker;K. Fogarty;D. Williams;F. Fay
通讯作者：
E. Moore;P. L. Becker;K. Fogarty;D. Williams;F. Fay
自发性高血压大鼠血管平滑肌细胞信号转导的改变。
DOI：
10.1161/01.hyp.19.2_suppl.ii142
发表时间：
1992
期刊：
Hypertension (Dallas, Tex. : 1979)
影响因子：
--
作者：
Bendhack,LM;Sharma,RV;Bhalla,RC
通讯作者：
Bhalla,RC
影响因子：
9.8
作者：
Nietgen, GW;Hönemann, CW;Durieux, ME
通讯作者：
Durieux, ME