Griendling K K, Berk B C, Ganz P, Gimbrone M A, Alexander R W
Hypertension. 1987 Jun;9(6 Pt 2):III181-5. doi: 10.1161/01.hyp.9.6_pt_2.iii181.
Phosphoinositide hydrolysis is an integral step in the activation of vascular smooth muscle by angiotensin II. Sequential phospholipase C-mediated hydrolysis of the polyphosphoinositides and phosphatidylinositol in cultured vascular smooth muscle cells stimulated with angiotensin II results in a coordinated series of biochemical events: a transient formation of inositol trisphosphate associated with calcium mobilization, and a biphasic, sustained formation of diacylglycerol associated with activation of protein kinase C and cytosolic alkalinization. The initial, rapid phase and the sustained phase of the angiotensin II response appear to be differentially controlled. Formation of inositol trisphosphate and mobilization of calcium are attenuated by activation of protein kinase C. Sustained diacylglycerol formation is promoted by cytosolic alkalinization, and appears to require cellular processing of the angiotensin II-receptor complex. Calcium and cyclic guanosine 3',5'-monophosphate do not appear to regulate phospholipase C-mediated phosphoinositide hydrolysis in vascular smooth muscle. Thus, regulation of angiotensin II-stimulated second messenger generation in vascular smooth muscle is complex, perhaps involving protein kinase C activation, changes in intracellular pH, and processing of the angiotensin II-receptor complex.
磷酸肌醇水解是血管紧张素II激活血管平滑肌过程中的一个重要步骤。在用血管紧张素II刺激培养的血管平滑肌细胞时，磷脂酶C介导的多磷酸肌醇和磷脂酰肌醇的顺序水解会导致一系列协同的生化事件：与钙动员相关的肌醇三磷酸的瞬时形成，以及与蛋白激酶C激活和胞质碱化相关的双相、持续的二酰基甘油形成。血管紧张素II反应的初始快速阶段和持续阶段似乎受到不同的控制。蛋白激酶C的激活会减弱肌醇三磷酸的形成和钙的动员。胞质碱化促进二酰基甘油的持续形成，并且似乎需要对血管紧张素II受体复合物进行细胞内加工。钙和环鸟苷3',5'-单磷酸似乎不调节血管平滑肌中磷脂酶C介导的磷酸肌醇水解。因此，血管紧张素II刺激的血管平滑肌中第二信使生成的调节是复杂的，可能涉及蛋白激酶C激活、细胞内pH值变化以及血管紧张素II受体复合物的加工。
