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维生素D3引起大鼠血管钙超载对血管L |
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李 夏 闫 宁 陈劲松 张连元 唐朝枢
摘 要 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（Vit D3）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(94.4±18.8)vs对照(10.7±1.8)μmol/g干重,(P＜0.01)，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50.5%和45.8%(P＜0.01)。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＜ 0.01)，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。
主题词 钙；血管；精氨酸；一氧化氮
Effects of vitamin D3 induced calcium overload on vascular
L-arginine/NO pathway in rat
LI Xia, YAN Ning, CHEN Jing-Song, ZHANG Lian-Yuan, TANG Chao-Shu
Dept. of Pathophysiology, Shanxi Staff Medical College, Taiyuan(030012)
Abstract AIM：To study the effects of calcium-overload on vascular L-arginine/NO (nitric oxide) pathway.METHODS：Changes of vascular NO production, cGMP content, L-citrulling conversion and L-arginine transport in vitamin D3 induced calcium-overload rat model were investigated, in comparison with the treated rats of oral administration of L-arginine.RESULTS：Vascular NO production and tissue cGMP content reduced in vitamin D3 induced calcium-overload rat model (vascular calcium content was 94.4±18.8 vs 10.7±1.8 μmol/g DW,P＜0.01), but L-citrulling conversion increased (P＜0.01).Vmax of high and low affinitive L-arginine transport decreased about 50.5% and 45.8% respectively (P＜0.01). Oral adiminstration of L-arginine improved vascular NO production, cGMP content (P＜0.01) and Vmax of L-arginine transport.CONCLUSION：Calcium overload cause injury of L-arginine transport in vascular L-arginine/NO pathway, and supplement of NO precursor may reduced the injury of calcium overload to vasculature.
MeSH Calcium; Blood vessels; Arginine; Nitric oxide
心血管钙超载是高血压、动脉硬化和粥样硬化的共同表现，亦是引起动脉斑块发生狭窄的重要因素之一［1］。钙超载的血管僵硬性增强、舒张功能降低的机制目前尚未完全阐明。血管内皮衍化舒张因子(endo thelium-derived relaxing factor/nitric oxide, EDRF/NO)是调节血管张力最重要[1] [2] 下一页
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