论文部分内容阅读
研究一种来自红细胞的新的内源性降压因子（ＥＤＤＦ）的降压机制，重点探讨其对血管平滑肌细胞（ＶＳＭＣ）胞浆游离钙离子（［Ｃａ~２＋］ｉ）及核内钙离子（［Ｃａ~２＋］ｎ）转运的影响．以 ｆｌｕｏ－３／ＡＭ作为 Ｃａ２＋~荧光探针，采用激光扫描共聚焦显微镜观察人脐静脉ＶＳＭＣ（ＨＵＶ），钙超载模型大鼠肠系膜ＶＳＭＣ（ＣａＯＭＶ）和正常对照 Ｗｉｓｔａｒ大鼠肠系膜培养的 ＶＳＭＣ（ＷＭＶ）（［Ｃａ~２＋］ｉ）及（［Ｃａ~２＋］ｎ）的变化；用流式细胞仪测定细胞周期和凋亡．结果表明：（１）ＥＤＤＦ可通过阻断ＶＳＭＣ质膜上的Ｌ型电压依赖性ａ~２＋通道（Ｌ－ｖｏｌｔａｇｅ ｄｅｐｅｎｄｅｎｔ ｃａｌｃｉｕｍ ｃｈａｎｎｅｌ，Ｌ－ＶＤＣ）和Ｒ型电压依赖性Ｃａ~２＋通道（Ｒ－ｖｏｌｔａｇｅｄｅｐｅｎｄｅｎｔ ｃａｌｃｉｕｍ ｃｈａｎｎｅｌ， Ｒ－ＶＤＣ）的开放，抑制胞外 Ｃａ~２＋内流，并可促进胞内 Ｃａ~２＋外流；（２） ＥＤＤＦ可明显抑制三磷酸肌醇（Ｉｎｏｓｉｔｏｌ－１，４，５－ｔｒｉｓｐｈｏｓｐｈａｔｅ，ＩＰ_３）敏感的胞内钙池的释放，促进胞内钙池的重储，但它对胞内 ｒｙａｎｏｄｉｎｅ敏感钙池的释放无抑制作用；（３） ＥＤＤＦ可增加肌浆网（ＳＲ
To study the antihypertensive mechanism of a new endogenous factor (EDDF) from erythrocytes and to investigate its effect on cytosolic free calcium ([Ca ~ 2 +] i) and intracellular calcium in vascular smooth muscle cells (VSMCs) ([Ca ~ 2 +] n) transport. Using fluo-3 / AM as a Ca2 + -fluorescence probe, we observed the proliferation of mesenteric VSMCs (WMV) in human umbilical vein (VSMC), calcium overload model rat mesentery VSMC (CaOMV) and normal control Wistar rats by laser scanning confocal microscopy ) ([Ca ~ 2 +] i) and ([Ca ~ 2 +] n). Cell cycle and apoptosis were determined by flow cytometry. The results showed that: (1) EDDF could block the expression of L-voltage dependent calcium channel (L-VDC) and R-type voltage dependent Ca 2+ channel (R- (2) EDDF can significantly inhibit Inositol-1, 4, 5- (3) EDDF can increase the sarcoplasmic reticulum (SR) release (SR), release of intracellular Ca (2+)