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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。
To investigate the possible mechanism of myocardial toxicity of parathyroid hormone PTH, we measured the release of 6-keto-PGF_ (-1α) from cardiomyocytes. The results showed that bPTH (1-34) significantly increased the release of PGI_2 in cardiomyocytes, which was dose-dependent. Calcium carrier A_ (23187) also stimulated the release of PGI_2 from cardiomyocytes; calcium complexing agent EDTA, calcium channel blocker Vera Pamir significantly inhibited; verapamil can also block the bPTH (1-34) PGI 2 release increased. These results suggest that the effect of PTH on the synthesis of PGI_2 by cardiomyocytes is influenced by intracellular Ca 2+. The significance of bPTH (1-34) increasing cardiomyocyte PGI 2 synthesis may be related to its interference with energy metabolism and cell damage.