Brunini Tatiana M C, Mendes-Ribeiro Antônio C, Ellory John C, Mann Giovanni E
Departamento de Farmacologia e Psicobiologia, Universidade do Estado do Rio de Janeiro, Rio de Janeiro 20550-030, Brazil.
Cardiovasc Res. 2007 Jan 15;73(2):359-67. doi: 10.1016/j.cardiores.2006.09.019. Epub 2006 Sep 30.
L-arginine is the physiological precursor for nitric oxide (NO) synthesis, and availability and transport of L-arginine modulate the rates of NO biosynthesis in circulating blood cells and the vasculature. NO is involved in many vascular functions such as vasodilation and inhibition of platelet aggregation and adhesion. We have established that reduced plasma L-arginine and NO production and increased tumour necrosis factor-alpha (TNF-alpha), fibrinogen, and C-reactive protein levels in malnourished uremic patients are associated with increased aggregability of platelets. Our findings may explain the increased cardiovascular mortality in patients with deficient nutritional status, leading to inflammation, oxidative stress, impaired L-arginine-NO signalling, and platelet activation. The aim of this review is to evaluate whether disturbances in the L-arginine-NO signalling pathway in chronic renal failure and atherosclerosis are affected by malnutrition and inflammation. We have included a brief overview of membrane transporters mediating influx of L-arginine and other cationic amino acids, as these transporters are involved in the potential benefits of L-arginine supplementation and platelet function in malnourished uremic patients.
L-精氨酸是一氧化氮（NO）合成的生理前体，L-精氨酸的可用性和转运调节循环血细胞和脉管系统中NO生物合成的速率。NO参与许多血管功能，如血管舒张以及抑制血小板聚集和黏附。我们已经证实，营养不良的尿毒症患者血浆L-精氨酸和NO生成减少，肿瘤坏死因子-α（TNF-α）、纤维蛋白原和C反应蛋白水平升高，这与血小板聚集性增加有关。我们的研究结果可能解释了营养状况不佳的患者心血管死亡率增加的原因，这会导致炎症、氧化应激、L-精氨酸-NO信号传导受损以及血小板活化。这篇综述的目的是评估慢性肾衰竭和动脉粥样硬化中L-精氨酸-NO信号通路的紊乱是否受营养不良和炎症的影响。我们简要概述了介导L-精氨酸和其他阳离子氨基酸流入的膜转运蛋白，因为这些转运蛋白与补充L-精氨酸的潜在益处以及营养不良的尿毒症患者的血小板功能有关。
