Ca^(2+)运动对α_1-肾上腺素受体引起内源性ClC-3氯通道表达的作用  

The relationship between Ca^(2+) movement and ClC-3 chloride channel expression induced by α_1-adrenoceptor

作　　者：王雪融[1] 关永源[1] 贺华[1] 丘钦英[1] 王冠蕾[1] 杨晓茹[1] 李沛波[1] 

机构地区：[1]中山大学中山医学院药理学教研室,广州510089

出　　处：《中国药理学通报》2003年第2期156-160,共5页Chinese Pharmacological Bulletin

基　　金：国家自然科学基金 (No 39970 849);广东省自然科学基金团队项目CMB(No 0 0 730 );国家科技部攀登计划项目 (No [1999] 0 5 4)资助

摘　　要：目的　研究Ca2 +运动对α1 肾上腺素受体引起ClC 3氯通道表达的作用。方法　在A10细胞上 ,用RT PCR和Westernblot检测ClC 3mRNA和蛋白质表达情况。结果　苯肾上腺素 ( 10 μmol·L-1)和thapsigargin( 0 1μmol·L-1)可促进ClC 3mRNA和蛋白质的表达 ;SK&F963 65 ( 10 μmol·L-1)和genistein( 10 μmol·L-1)可抑制苯肾上腺素引起的ClC 3的表达 ,nifedipine( 10 μmol·L-1)无此作用。结论　在A10细胞上 ,通过钙池操纵性Ca2 +通道 (SOCC)的Ca2 +内流参与了α1 肾上腺素受体引起的内源性ClC 3氯通道的表达 ,而通过电压依赖性Ca2 +通道 (VDCC)的Ca2 +内流可能与此无关。蛋白酪氨酸激酶参与了ClCAIM To investigate the relationship between Ca 2+ movement and ClC-3 chloride channel expression induced by α 1-adrenoceptor. METHODS RT-PCR and Western blot were used to test the mRNA and protein expression of ClC-3 in A10 cells. RESULTS Phenylephrine(10 μmol·L -1) and thapsigargin(0.1 μmol·L -1) induced ClC-3 expression. SK&F96365(10 μmol·L -1) and genistein(10 μmol·L -1) inhibited ClC-3 expression induced by phenylephrine(10 μmol·L -1), while nifedipine(10 μmol·L -1) had no effect. CONCLUSION Calcium-operated Ca 2+ channel(SOCC) contributes to ClC-3 chloride channel expression induced by α 1-adrenoceptor, while voltage-dependent Ca 2+ channel(VDCC) might have no effect. Protein tyrosine kinase has some role in ClC-3 expression.

关 键 词：Α1-肾上腺素受体 CLC-3 氯通道 CA^2+通道 

分 类 号：R977.1[医药卫生—药品]