甲状旁腺素增加心率的机制研究  

Mechanism for Increasing Heart Rate Mediated by Parathyroid Hormone

作　　者：郑燕倩[1] 李慈珍[1] 张颖[1] 刘远谋[1] 

机构地区：[1]上海第二医科大学基础医学院生理学教研室,上海200025

出　　处：《上海第二医科大学学报》2005年第6期549-552,共4页Acta Universitatis Medicinalis Secondae Shanghai

基　　金：国家自然科学基金(30270498);上海市卫生局基金(024078)资助项目.

摘　　要：目的研究甲状旁腺素(PTH)增加心率的机制。方法运用微电极、膜片箝技术,记录PTH对家兔自律性动作电位和兔起搏离子流的影响。结果2×10-7mol/Lnifedipine使窦房结细胞动作电位的幅值减小及自律性减慢(P<0.05)。PTH20nmol/L增加窦房结动作电位的自律性及动作电位幅值的作用可被nifedipine减弱(P<0.05)。PTH10nmol/L使酶解游离窦房结细胞起搏离子流(If)明显增加。结论甲状旁腺素通过增强窦房结细胞起搏离子流If及钙内流来增加窦房结的自律活动。Objective To investigate the mechanism of parathyroid hormone(PTH) to induce the fast heart rate.Methods Conventional microelectrode and patch clamp techniques were used to record the PTH-induced changes of action potential and pacemaker current I f in the rabbit sinus node. Results Nifedipine 2×10 -7 mol/L could decrease the amplitude and spontaneous depolarization rate of sinus node action potential(P<0.05). PTH could increase the amplitude and spontaneous depolarization rate of SN action potential, which could be partially reversed by nifedipine (P<0.05). The pacemaker current I f was increased significantly by PTH 10nmol/L. Conclusion The positive chronotropic effect of PTH is mediated by its enhancing Ca 2+ inward current and pacemaker current I f.

关 键 词：甲状旁腺素 NIFEDIPINE 机制研究 心率 起搏离子流 mol/L 自律性动作电位 窦房结细胞 细胞动作电位 膜片箝技术 PTH 微电极 钙内流 

分 类 号：R33[医药卫生—人体生理学]