【摘要】 尿酸(UA)是人体内嘌呤代谢的最终产物，其代谢紊乱会诱发高尿酸血症(HUA)。HUA的发生和发展与氧化应激损伤、炎症因子激活、肾素-血管紧张素-醛固酮系统激活等诸多病理机制密切相关，这些机制直接或间接影响着机体对内源性一氧化氮(NO)的生物利用度。此外，在以高浓度UA为独立危险因素的疾病中，普遍存在NO生物利用度降低的现象。本文对高浓度UA影响机体内源性NO生物利用度的机制进行综述，重点总结了高浓度UA使NO合成减少和/或消耗增加的机制，以期为临床更好地改善HUA多系统症状和预后提供参考，为深入研究HUA与其他代谢性疾病的相关性提供理论依据。更多还原

【Abstract】 Uric acid(UA) is the final product of purine metabolism in human body, and its metabolic disorder will induce hyperuricemia(HUA).The occurrence and development of HUA are associated with a variety of pathological mechanisms such as oxidative stress injury, activation of inflammatory cytokines, and activation of renin-angiotensin-aldosterone system.These mechanisms directly or indirectly affect the bioavailability of endogenous nitric oxide(NO).The decrease in NO bioavailability is common in the diseases with high concentration of UA as an independent risk factor.In this review, we summarize the mechanisms by which high concentrations of UA affect the endogenous NO bioavailability, with a focus on the mechanisms of high-concentration UA in decreasing the synthesis and/or increasing the consumption of NO.This review aims to provide references for alleviating the multisystem symptoms and improving the prognosis of HUA,and lay a theoretical foundation for in-depth study of the correlations between HUA and other metabolic diseases.更多还原