甲状旁腺素对心肌细胞Ca^(2+)跨膜转运的影响

Effects of parathyroid hormone on calcium transsacolemma in cultured heart cells

应用放射性同位素^(45)Ca示踪技术观察了牛甲状旁腺素_(1-34)活性片段(bPTH_(1-34))对培养乳鼠心肌细胞钙离子(Ca^(2+))跨膜转运的影响.并且镜检了细胞的搏动频率和采用蛋白质竞争结合法检测了胞内cAMP的含量。结果表明:bPTH_(1-34)(1×10^(-7)mol·L^(-1))显著增加静息细胞的搏动频率.明显增高细胞cAMP的含量.并且显著增加静息、高K^+去极化及NA受体兴奋状态细胞的外Ca^(2+)内流.同时抑制胞内Ca^(2+)外排。提示其强心与细胞内Ca^(2+)升高的机理之一.可能与细胞内cAMP升高有关。

In order to obtain some evidences of the role of parathyroid hormone (PTH) in regulating calcium metabolism, and explore the mechanisms by which PTH regulates calcium in the heart, 45Ca was used to study the influence of bovine PTH1-34 fragment (bPTH1-34) on calcium transsacolemma. The results indicate that bPTH1-34(l×I0-7mol · L-1) increases beating rate of heart cells under normal state and it markedly increases the rapid (5 min) and the slow (120 min) phases of 45Ca influx in heart cells (under normal, KC1 10-5 mol·L-1 high K+depolarised, NA 10-7mol·L-1receptors activated states), but it could also reduce 45Ca efflux from the cultured heart cells. It suggests that the mechanisms caused by bPTH1-34 which enhances the cytosolic calcium concentration and myocardial beating rate may be related with cAMP level elevated in heart cells.