中文摘要：

为了探讨钙库活化的钙通道（store-operatedcalciumchannels，soc）和受体活化的钙通道（receptor-operatedcalciumchan．nels，ROC）在人脐静脉内皮细胞（humanumbilicalveinendothelialcell，HUVEC）钙敏感受体（Ca2＋-sensingreceptor,CaR）介导的钙内流及NO生成中的作用和机制，本实验通过分别或联合使用SOC阻断剂、非选择性的阳离子通道阻断剂、ROC激动剂和ROC阻断剂，采用Fura·2／AM检测细胞内钙离子浓度（intracellularCa2’concentration，[Ca2＋]i）变化，NO荧光探针DAF．FMDA测定细胞内内皮型一氧化氮合酶（endothelialnitricoxidesynthase，eNOS）活性和N0生成的变化。结果显示，与对照组（Spermine＋ca2＋组，激活CaR）相比，单独阻断SOC或ROC，HUVEC中[ca2＋]、eNOS活性和NO含量均降低（P〈0．05），而ROC激动剂可部分取消ROC阻断剂的阻断作用俨〈0．05），SOCSDROC联合阻断可进一步加强上述抑制作用妒〈0．05）。上述结果表明，在Spermine刺激活CaR介导[Ca2＋]i、eNOS活性~IINO的生成过程中，soc和ROC以协同的方式参与了CaR介导的钙内流及NO生成。

英文摘要：

This paper aims to investigate the effect of store-operated calcium channels （SOC） and receptor-operated calcium channels （ROC） on Ca2＋-sensing receptor （CaR）-induced extracellular Ca2＋ influx and nitric oxide （NO） generation in human umbilical vein endothelial cells （HUVEC）. SOC blocker, non-selective cation channel blocker, ROC agonist and ROC blocker were used separately and combined. Intracellular Ca2~ concentration （[Ca：~]i） was measured by Fura-2/AM loading. The activity of endothelial nitric oxide synthase （eNOS） and the production of NO were determined by the DAF-FM diacetate （DAF-FM DA）. The results showed that increases of [Ca2＋]~, eNOS activity and NO generation induced by CaR agonist Spermine were all reduced after single blocking the SOC or ROC, respectively （P 〈 0.05）. ROC agonist can partially abolish the ROC blocker＇s effect （P 〈 0.05）. The above mentioned effects evoked by CaR agonist Spermine were further reduced when blocking both SOC and ROC than single blocking SOC or ROC in HUVEC （P 〈 0.05）. In conclusion, these results suggest that the SOC and ROC participate in the processes of CaR-evoked extra-cellular Ca2＋ influx and NO generation by a synergistic manner in HUVEC.