【摘要】 目的 通过肾阳虚模型血浆内皮素、一氧化氮含量的变化，而探索“阳虚则寒”寒证的分子机制，以进一步明确肾阳虚证的物质基础。方法 用腺嘌呤灌胃复制小鼠肾阳虚模型，通过硝酸还原酶法和放射免疫法分别检测血浆一氧化氮(NO)和内皮素(ET)的含量，并用SPSS12.0软件统计分析。结果 肾阳虚组血浆内皮素含量高于正常对照组 (P<0.05), 一氧化氮低于正常对照组，但两组比较无统计学意义(P>0.05)。结论 肾阳虚时机体血浆ET水平升高而导致的分别以ET、NO为主的缩血管与舒张血管因素动态平衡失调为“阳虚则寒”寒证的分子机制之一。

    【关键词】 肾阳虚; 阳虚则寒; 一氧化氮; 内皮素

    The molecular mechanism study on the cold syndrome of the yang asthenia causing cold theory--changes of ET and NO in plasma of the mice with renal yang asthenia syndrome

    LIU Xin, LAN Jin Mei, LI Dong Mei, et al. Guizhou Zunyi School of Traditional Chinese Medicine，Zunyi 563004, China

    【Abstract】 Objective To explore the molecular mechanism of the cold syndrome of the yang asthenia causing cold，for finding out furtherly the material basis of renal yang asthenia syndrome by changs of ET and NO levels in plasm of the mouse models with renal yang asthenia syndrome. Methods To establish the mouse model of renal yang asthenia syndrome by perfusing the stomach with adenine 30mg/100g.body weight.d continuously for 30 days and detect the ET and NO levels in plasma on the last day, and then,process these data by SPSS 12.0. Results Levels of ET were significantly higher in plasma of the renal yang asthenia mice than those of the nomal-control and levels of NO were lower but insignificantly.Conclusion It is the one of the cold-syndrome molecular mechanism of the yang asthenia causing cold theory that cause the dynamic imbalance of vasoconstrictor and vasodilator factors respectively represented by levels of ET and NO in blood due to ET overexpression in renal yang asthenia syndrome. ......