呋塞米对α_1肾上腺素受体亚型引起的Ca^(2+)内流的影响  

Effects of furosemide on Ca^(2+) influx induced by α_1^-adrenoceptor subtypes

作　　者：李劲梁[1] 关永源[1] 韩启德[2] 贺华[1] 丘钦英[1] 

机构地区：[1]中山医科大学药理学教研室,广州510089 [2]北京医科大学第三医院血管医学研究所,北京100083

出　　处：《中国药理学通报》2000年第1期32-36,共5页Chinese Pharmacological Bulletin

基　　金：国家自然科学基金!(No39770858);香港求是科技基金资助课题

摘　　要：目的　探讨Cl-通道开放在不同α1肾上腺素受体亚型引起的Ca2 +内流中的作用。方法　采用Fura 2 /AM荧光分光光度法 ,测定胞浆游离Ca2 +浓度 ,观察Cl-通道阻断剂呋塞米 ,钙通道阻断剂SK&F96 36 5和硝苯地平对不同α1肾上腺素受体亚型 (α1A、α1B AR)引起的Ca2 +内流的影响 ,并加以比较。结果　 2 5 ,5和 10 μmol·L-1呋塞米呈浓度依赖性地抑制了α1A和α1B AR亚型引起的Ca2 +内流 ;对α1A AR引起的Ca2 +内流的抑制率分别为 8 3 %± 6 1% ,2 3 8%±14 8%和 40 7%± 19 3% ,对α1B AR引起的Ca2 +内流的抑制率分别为 12 0 %± 5 4% ,19 2 %± 4 9%和 31 9%±4 9%。α1A AR引起的Ca2 +内流被最大抑制浓度 ( 2 0 μmol·L-1)的SK&F96 36 5抑制后 ,不能被 10 μmol·L-1呋塞米进一步抑制 ;而α1B AR引起的Ca2 +内流被 2 0 μmol·L-1SK&F96 36 5抑制后 ,仍能被 10 μmol·L-1呋塞米进一步抑制 ,抑制率为 6 6 %± 3 2 %。结论　参与α1A和α1B AR引起的Ca2AIM To investigate the roles of Cl- channels in Ca 2+ influx induced by activation of α 1adrenoceptor subtypes METHODS With Fura2/AM spectrophotofluorometry, the effects of furosemide, SK&F96365 and nifedipine on α 1A and α 1B AR induced Ca 2+ influx were determined RESULTS 25, 5 and 10 μmol·L -1 furosemide inhibited both α 1A and α 1B AR induced Ca 2+ influx in a concentrationdependent fashionThe inhibition rates were 83%±61%,238%±148%, 407%±193% forα 1A AR and 120%±54%,192%±49%,319%±49% for α 1B AR, respectively α 1A AR induced Ca 2+ influx which had been inhibited by 20 μmol·L -1 SK&F96365 could not be inhibited by 10 μmol·L -1 furosemide, whereas α 1B AR induced Ca 2+ influx which had been inhibited by 20 μmol·L -1 SK&F96365 could be further inhibited by 10 μmol·L -1 furosemide by 66%±32% CONCLUSION The characteristics of Cl- channels related to α 1A and α 1B ARinduced Ca 2+ influx are different

关 键 词：呋塞米 Α1肾上腺素受体亚型 游离钙 氯通道 

分 类 号：R972[医药卫生—药品]