高尿酸血症与高血压病相关性的研究进展

尿酸是人体内嘌呤代谢的最终产物,当尿酸生成增多和/或排出减少时,均可引起血中尿酸盐浓度增高。当血尿酸水平男性大于7.0 mg/dl,女性大于6.0 mg/dl称为高尿酸血症。作为嘌呤代谢紊乱所致疾病,高尿酸血症以往仅侧重于痛风性关节炎、痛风石沉积和肾尿酸结石形成等的诊断与治疗。目前新近研究表明:高尿酸血症可能是高血压病的独立危险因素之一且尿酸水平增高通常早于高血压的发生与进展,干预尿酸水平有望成为高血压治疗的新靶点,随着高血压研究的全球化深入,对于尿酸及尿酸水平增高的流行病学、基础学与临床方面的研究也日益备受关注。基于此,本文对尿酸的合成与代谢;高尿酸血症成因及其与高血压的流行病学研究;高尿酸血症通过引发一氧化氮合成水平减低、血管平滑肌细胞生物学行为改变、机体炎症与氧化应激反应及肾素-血管紧张素系统激活等方面所致高血压的发病机制;高尿酸血症干预治疗对于高血压病的转归进行简要综述。

Research Progress of Uric Acid, Hyperuriemia and Hypersion

Uric acid is the naturally occurring product of purine metabolism. Hyperuricemia was defined as more than 7mg perdeciliter in men and more than 6mg per deciliter. Hyperuricemia is the major etiological factor of gout and kidney disease. Recent experimental and clinical evidence notes the possibility that an elevated level of uric acid may lead to the development of hypertension andmay be an independent risk factor for hypertension. This review summarizes metabolism of urid and acid, the causes of hyperuricemia,epidemiology of uric acid and hypertension, hyperuricemia in the role of hypertension. Hyperuricemia may be a new therapeutic targe inthe prevention and treatment of hypertension.