摘要
采用Fura 2荧光测定胞浆游离Ca2 + 浓度([Ca2 + ]i)变化技术 ,在培养的牛脑中动脉平滑肌细胞上 ,观察电压依赖Ca2 + 通道 (VDCC)抑制药尼莫地平 ,非电压依赖Ca2 + 通道 (NVDCC)SK&F96365以及Cl-通道抑制药呋塞米 ,印防己毒素对ATP引起的[Ca2 + ]i 反应的影响 .实验表明ATP可使 [Ca2 + ]i 呈现双相升高反应 ,即快速峰相及随后持续稳定的平台相 .尼莫地平 ,SK&F96365及印防己毒素对ATP触发的Ca2 + 内流无明显影响 ,而呋塞米能呈浓度依赖性地抑制ATP触发的Ca2 + 内流 .提示ATP触发的牛脑中动脉平滑肌细胞Ca2 + 内流是经SK&F96365不敏感的NVDCC ,与呋塞米敏感的Cl- 通道开放有关 .
In order to understand the ATP-induced Ca 2+ influx characterization, we studied the effects of Ca 2+ channel blockers(nimodipine and SK&F96365) and Cl - channel blockers(furosemide and picrotoxin) on ATP-induced influx in cultured calf middle cerbral artery smooth muscle cells, with Fura-2 fluorescence technique. ATP evoked the increase in cytoplasmic Ca 2+( i) level. The response to ATP was biphasic, a transient peak followed by a sustained plateau. This sustained plateau was not significantly reduced by (1) voltage-dependent Ca 2+ channel(VDCC) blocker nimodipine; (2) receptor-operated Ca 2+ channel(ROCC) blocker SK&F96365; (3) Cl - channel blocker picrotoxin. However, it was significantly inhibited by furosemide in a concentration-dependent manner. These data suggest that ATP-induced Ca 2+ influx be related to NVDCC, which is not sensitive to SK&F96365, instead of the VDCC, and furosemide-sensitive Cl - channel is related to this Ca 2+ influx.
出处
《中国药理学与毒理学杂志》
CAS
CSCD
北大核心
2001年第5期347-352,共6页
Chinese Journal of Pharmacology and Toxicology
基金
国家自然科学基金资助项目 (39970 849)
广东省自然科学基金资助项目 (省字 :98 30 2 )
美国纽约人寿国际公司资助项目~~
关键词
氯通道
脑动脉
氯通道
腺苷三磷酸
尼莫地平
呋塞米
钙通道
血管平滑肌细胞
cells, cultured
muscle, smooth, vascular
cerebral arteries
calcium, cytosolic
chloride channels
adenosine triphosphate
nimodipine
furosemide
