摘要
目的:研究动脉平滑肌细胞内钙池耗竭所致浆膜钙通透性的增加.方法:在无钙条件下,采用选择性肌浆网(SR)钙泵抑制剂环匹阿尼酸(CPA)和Thapsigargin(Tha)及SR钙释放剂Ryanodine(Rya)耗竭家兔主动脉环咖啡因和苯肾上腺素敏感的细胞内钙池,而当外钙加入时,以上三药均增大基础张力,此张力变化做为内钙耗竭后所致的浆膜钙通透性增加.结果:3 μmol·L^(-1) Tha和Rya及30 ^(-1)mol·L^(-1)CPA分别增加张力为0.94,1.1和0.14 g,Rya的张力增加不受CPA抑制.结论:(1)提示除细胞内钙耗竭外,SR钙通道开放也增加浆膜钙通透性;(2)Rya完全开放钙通道需咖啡因的存在.
AIM: To study the increase of plasma membrane Ca24 permeability in response to depletion of intracellular Ca2+ stores. METHODS:In Ca2+-free medium, 2 selective inhibitors of sarcoplasmic reticulum (SR) Ca2+ pump ATPase, cyclopiazonic acid (CPA) and thapsigargin (Tha), and an activator of Ca2+-induced Ca2+ release channel (CICR), ryan-odine (Rya ), depleted intracellular Ca2+ stores sensitive to both caffeine and phenyle-phrine in rabbit aortic rings and caused sustained tensions when Ca2+ reintroduction. These tensons were taken as the increase of plasma Ca2+ permeability by depletion of intracellular Ca2+ stores. RESULTS: The extracellular Ca2+-dependent tensions causedby Tha and Rya 3 umol.L-1 and CPA 30 .L-1 were 0. 94, 1.1, and 0. 14 g, respectively , and the tension caused by Rya was not inhibited by CPA. CONCLUSION: (a) Besides the depletion of intracellular Ca2+ stores, an activated state of Ca2+ release channels in SR may also mediate the activation of Ca2+ influx from plasma membrane in rabbit aorta; (b) Rya needs caffeine to fully open CICR channel in SR.
出处
《中国药理学报》
CSCD
1995年第3期280-284,共5页
Acta Pharmacologica Sinica
关键词
环匹阿尼酸
胸主动脉
咖啡因
苯福林
cyclopiazonic acid
thapsigargin
ryanodine
thoracic aorta
caffeine
phenylephrine
