甲状旁腺激素对心肌细胞PGI_2释放的影响  

INFLUENCE OF bPTH ( 1-34 ) ON PGI_2 RELEASE FROM HEART CELLS

作　　者：张一彬[1] 王振纲[1] 程锦轩[1] 

机构地区：[1]中国医学科学院基础医学研究所药理教研室,北京100005

出　　处：《中国药理学通报》1991年第3期197-200,共4页Chinese Pharmacological Bulletin

摘　　要：为探讨甲状旁腺激素PTH心肌毒性的可能机制,我们对心肌细胞释放6-keto-PGF_(-1α)进行了测定。结果表明,bPTH(1-34)明显增加心肌细胞释放PGI_2,该作用与剂量有关;钙载体A_(23187)也能刺激心肌细胞释放PGI_2;钙离子络合剂EDTA,钙通道阻断剂维拉帕米明显抑制之;维拉帕米还可阻断bPTH(1-34)对PGI_2释放的增加作用。提示PTH促进心肌细胞合成PGI_2的作用受细胞内外钙离子的影响。bPTH(1-34)增加心肌细胞PGI_2合成的意义可能与其干扰能量代谢进而使细胞损伤有关。In order to explore the mechanism of cardiac damage by PTH, the release of PGI2 from heart cells was measured. The results showed that bPTH ( 1-34) increased the release of 6-keto-PGFla from heart cells in a dose dependent manner. Calcium inophone A23187 also increased the 6-keto-PGF1α release, while EDTA and verapamil reduced it. These suggest that the PGI2 synthesis in heart cells was affected by intra and extracellular calcium. The significance of bPTH( 1-34) induced increase of PGI2 synthesis might be associated with interference of energy metabolism, and then, cell damage.

关 键 词：甲状腺激素 心肌细胞 维拉帕米 

分 类 号：R965.1[医药卫生—药理学]