INTRACELLULAR CALCIUM-CONCENTRATION IN VASCULAR SMOOTH-MUSCLE CELLS OF RATS WITH CIRRHOSIS
INTRACELLULAR CALCIUM-CONCENTRATION IN VASCULAR SMOOTH-MUSCLE CELLS OF RATS WITH CIRRHOSIS
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DOI：
10.1016/s0168-8278(94)80096-0
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发表时间：
1994-10-01
影响因子：
25.7
通讯作者：
RODES, J
中科院分区：
文献类型：
--
作者：
CASTRO, A;ROS, J;RODES, J
对内源性血管收缩剂（如血管紧张素 II 和加压素）的加压反应降低是肝硬化腹水的特征性表现；这被认为是造成这种疾病中小动脉血管舒张的部分原因。先前的研究表明，这种异常是由于受体后缺陷导致细胞内 Ca2+ 动员改变所致。为了评估这一假设，分别在主动脉环和原代培养的主动脉血管平滑肌细胞中测量了基础条件下以及血管紧张素II（1-100 nM）和加压素（100 nM）刺激后血管对血管紧张素II（3.10（-8）M）和细胞内Ca2+浓度的反应。该研究在 43 只对照大鼠和 40 只患有 CCl4 诱导的肝硬化和腹水的大鼠中进行。细胞在玻璃盖玻片上生长至汇合，然后加载 Fura-2（一种荧光细胞内 Ca2+ 指示剂），用于连续监测细胞内 Ca2+ 浓度。与对照环相比，在肝硬化主动脉环中检测到收缩器对血管紧张素 II 的反应降低（张力增加：31+/-5 vs 79+/-14 mg，p
A decreased presser response to endogenous vasoconstrictors, such as angiotensin II and vasopressin, is a characteristic finding in cirrhosis with ascites; this has been considered as partially responsible for the arteriolar vasodilation present in this disease. Previous investigations suggested that this abnormality is due to a post-receptor defect leading to altered intracellular Ca2+ mobilization. To assess this hypothesis, vascular responsiveness to angiotensin II (3.10(-8) M) and intracellular Ca2+ concentration in basal conditions and following angiotensin II (1-100 nM) and vasopressin stimulation (100 nM) were measured in aortic rings and in primary cultured aortic vascular smooth muscle cells, respectively. The study was carried out in 43 control rats and 40 rats with CCl4-induced cirrhosis and ascites. Cells were grown to confluence on glass cover slips and then loaded with Fura-2, a fluorescent intracellular Ca2+ indicator, for continuous monitoring of intracellular Ca2+ concentration. A decreased constrictor response to angiotensin II was detected in cirrhotic aortic rings in comparison to control rings (increase in tension: 31+/-5 vs 79+/-14 mg, p