Alexander R W, Brock T A, Gimbrone M A, Rittenhouse S E
Hypertension. 1985 May-Jun;7(3 Pt 1):447-51.
Angiotensin II stimulated the breakdown of phosphatidylinositol-4,5-bisphosphate (PIP2) and the generation of inositol trisphosphate (IP3) in cultured rat aortic smooth muscle cells. The decrease in PIP2 and increase in IP3 levels were rapid (measurable at 5 seconds; maximum IP3 levels at 15 seconds). The time course of these changes was comparable to that of angiotensin II-induced increases in cytosolic free calcium, as measured by the calcium-sensitive fluorescent indicator quin 2. The IP3 formation was not stimulated by the calcium ionophore A23187 (5 microM), nor were angiotensin II-induced changes in IP3 formation inhibited by the removal of extracellular calcium with EGTA. Angiotensin II appears to be capable of generating more IP3 than is required for maximal release of intracellular calcium. These data are consistent with the hypothesis that generation of IP3 plays a role in the angiotensin II-induced mobilization of calcium from intracellular storage sites in vascular smooth muscle cells.
血管紧张素II刺激培养的大鼠主动脉平滑肌细胞中磷脂酰肌醇-4,5-二磷酸（PIP2）的分解并生成肌醇三磷酸（IP3）。PIP2水平降低和IP3水平升高迅速（5秒时可检测到；15秒时IP3水平达到最大值）。这些变化的时间进程与血管紧张素II诱导的胞质游离钙增加的时间进程相当，这是通过钙敏感荧光指示剂喹啉2测量的。IP3的形成不受钙离子载体A23187（5微摩尔）刺激，用乙二醇双（2-氨基乙基醚）四乙酸（EGTA）去除细胞外钙也不抑制血管紧张素II诱导的IP3形成变化。血管紧张素II似乎能够产生比细胞内钙最大释放所需更多的IP3。这些数据与IP3的生成在血管紧张素II诱导的血管平滑肌细胞内钙储存部位钙动员中起作用的假设一致。
