Takuwa Y, Masaki T, yamashita K
Department of Internal Medicine, University of Tsukuba, Ibaraki, Japan.
Contrib Nephrol. 1991;90:99-104. doi: 10.1159/000420130.
The mechanisms of actions were investigated in cultured rat aortic vascular smooth muscle A-10 cells. The A-10 cells have a single class of high affinity binding sites for ET with an apparent Mr of 65,000-75,000 on SDS-PAGE. Stimulation of cells with ET induces mobilization of Ca2+ from both intra- and extracellular pools to produce a biphasic increase in cytoplasmic free Ca2+ concentration. A dihydropyridine Ca2+ channel antagonist does not inhibit the second plateau phase of the [Ca2+]i increase which is dependent on extracellular Ca2+. ET stimulates phospholipase C to produce inositol trisphosphate and 1,2-diacylglycerol vai a pertussis toxin-insensitive G protein. These results indicate that the receptor activation by ET is coupled to phospholipase C activation and Ca2+ channel gating in vascular smooth muscle cells.
在培养的大鼠主动脉血管平滑肌A - 10细胞中研究了其作用机制。A - 10细胞对内皮素具有一类高亲和力结合位点，在SDS - PAGE上其表观分子量为65,000 - 75,000。用内皮素刺激细胞可诱导Ca2+从细胞内和细胞外钙库中动员出来，使细胞质游离Ca2+浓度呈双相增加。二氢吡啶类Ca2+通道拮抗剂并不抑制依赖细胞外Ca2+的[Ca2+]i增加的第二个平台期。内皮素刺激磷脂酶C通过一种对百日咳毒素不敏感的G蛋白产生肌醇三磷酸和1,2 - 二酰甘油。这些结果表明，内皮素激活受体与血管平滑肌细胞中的磷脂酶C激活和Ca2+通道门控相偶联。
