论文部分内容阅读
目的：观察血管钙超载对Ｌ－精氨酸／ＮＯ途径的影响。方法：维生素Ｄ３（ＶｉｔＤ３）注射引起大鼠血管钙超载，检测血管ＮＯ生成、ｃＧＭＰ含量、Ｌ－瓜氨酸转化及Ｌ－精氨酸转运的变化，并与口服Ｌ－精氨酸治疗组大鼠比较。结果：大鼠血管钙含量（９４４±１８８）ｖｓ对照（１０７±１８）μｍｏｌ／ｇ干重，（Ｐ＜００１），血管ＮＯ生成减少，组织ｃＧＭＰ含量降低，但Ｌ－瓜氨酸转化增高，Ｌ－精氨酸（Ｌ－Ａｒｇ）高和低亲和性转运的最大速率（Ｖｍａｘ）分别降低５０５％和４５８％（Ｐ＜００１）。口服Ｌ－Ａｒｇ治疗的大鼠血管ＮＯ生成和ｃＧＭＰ含量都较钙超载大鼠明显增高（Ｐ＜００１），Ｌ－Ａｒｇ高、低亲和性转运的Ｖｍａｘ增加。结论：血管钙超载对Ｌ－Ａｒｇ／ＮＯ途径损伤的主要环节在Ｌ－Ａｒｇ的跨膜转运，补充ＮＯ前体Ｌ－Ａｒｇ可能减轻钙超载引起的血管损伤。
Objective: To observe the effect of vascular calcium overload on L-arginine / NO pathway. Methods: Vitamin D3 (VitD3) injection caused vascular calcium overload in rats. The changes of NO production, cGMP, L-citrulline and L-arginine transport were detected. Comparison of rats. Results: Compared with the control group (944 ± 188) and control group (107 ± 18) μmol / g dry weight, the blood vessel NO production decreased and the cGMP content decreased , But the L-citrulline conversion increased, the maximum rate of L-Arg transport and low affinity transport (Vmax) decreased by 505% and 458% (P <001 ). Oral L-Arg treatment in rats NO production and cGMP levels were significantly higher than calcium overload rats (P <0 01), L-Arg high and low affinity transport Vmax increased. CONCLUSION: The main link of L-Arg / NO pathway damage is the translocation of L-Arg across the membrane. L-Arg, a NO precursor, may reduce vascular damage induced by calcium overload.