Rahimian R, Wang X, van Breemen C
Vancouver Vascular Biology Research Center (VVBRC), Canada.
Biochem Biophys Res Commun. 1998 Jul 30;248(3):916-9. doi: 10.1006/bbrc.1998.9068.
Intracellular Ca2+ concentration ([Ca2+]i) was measured by Fura 2/AM fluorescence imaging microscopy in freshly isolated valvular endothelial cells taken from female and male rats. The basal level of [Ca2+]i was significantly elevated in female valvular endothelial cells when compared to males (P < 0.05). Inhibition of the sarco-endoplasmic reticulum Ca(2+)-ATPase with cyclopiazonic acid (CPA, 10 microM) caused a greater increase in the [Ca2+]i in female than male endothelial cells. Removal of extracellular Ca2+ returned the [Ca2+]i to the basal level. The rate of [Ca2+]i decline was significantly slower in female endothelial cells compared to males. There were no differences in the unstimulated rate of Mn2+ quenching between two groups. These results demonstrate that estrogen affects NOS at least in part, by an alteration in Ca2+ homeostasis in endothelial cells.
采用Fura 2/AM荧光成像显微镜测量从雌性和雄性大鼠新鲜分离的瓣膜内皮细胞中的细胞内Ca2+浓度（[Ca2+]i）。与雄性相比，雌性瓣膜内皮细胞中[Ca2+]i的基础水平显著升高（P < 0.05）。用环匹阿尼酸（CPA，10 microM）抑制肌浆内质网Ca(2+)-ATP酶，导致雌性内皮细胞中[Ca2+]i的增加幅度大于雄性。去除细胞外Ca2+可使[Ca2+]i恢复到基础水平。与雄性相比，雌性内皮细胞中[Ca2+]i下降速率明显较慢。两组之间未刺激的Mn2+淬灭速率没有差异。这些结果表明，雌激素至少部分地通过改变内皮细胞中的Ca2+稳态来影响一氧化氮合酶。
