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.
出处
《中国药理学通报》
CAS
CSCD
北大核心
1991年第3期197-200,共4页
Chinese Pharmacological Bulletin
关键词
甲状腺激素
心肌细胞
维拉帕米
bPTH (1-34), Heart cells, Calcium inophone A23187, Verapamil, PGI_2, 6-keto-PGF_(1α)
