Perturbation of intracellular calcium ion concentration in single rat granulosa cells by angiotensin II.
Perturbation of intracellular calcium ion concentration in single rat granulosa cells by angiotensin II.
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血管紧张素 II 对单个大鼠颗粒细胞内钙离子浓度的扰动。
DOI：
10.1210/endo-124-2-1094
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发表时间：
1989
期刊：
影响因子：
4.8
通讯作者：
P. Leung
中科院分区：
文献类型：
--
作者：
J. Wang;K. Baimbridge;P. Leung
血管紧张素II（Ang II）对卵巢的生理作用最近已被提出，但其作用机制尚不清楚。在44个单独的大鼠颗粒细胞中，18个负载Fura-2，Ang II引起细胞内游离钙离子浓度（[Ca 2 +]i）的快速和短暂的增加。在其中12个细胞中，10（-5）M Ang II引起[Ca 2 +]i增加3.7 +/-0.5倍。74 +/- 4秒后，[Ca 2 +]i恢复至静息水平（96.0 +/- 3.7 nM）。血管紧张素I无效（n = 9）。Ang Ⅱ对[Ca ~（2+）]i变化的影响可被有效的长效Ang Ⅱ拮抗剂[Sar 1，Thr 8]-Ang Ⅱ完全阻断，提示其作用机制可能是受体介导的。目前的结果强烈表明，[Ca 2 +]i的快速变化是在大鼠卵巢细胞亚群中的血管紧张素II的信号转导的早期步骤。
A physiological role of angiotensin II (Ang II) on the ovary has been suggested recently, but the mechanism of action is not understood. In 18 out of 44 individual rat granulosa cells loaded with fura-2, Ang II caused a rapid and transient increase in intracellular free calcium ion concentration, [Ca2+]i. In 12 of these cells, 10(-5) M Ang II caused a 3.7 +/- 0.5-fold increase in [Ca2+]i. After 74 +/- 4 sec, [Ca2+]i returned to the resting levels (96.0 +/- 3.7 nM). Angiotensin I was without effect (n = 9). The effect of Ang II on [Ca2+]i changes could be completely blocked by a potent long-acting Ang II antagonist, [Sar1, Thr8]-angiotensin II, suggesting a receptor-mediated mechanism. The present results strongly indicate that rapid alterations in [Ca2+]i is an early step in the signal transduction of Ang II in a subpopulation of cells in the rat ovary.