Uric acid is the final product of purine metabolism, and its increased serum levels have been directly involved in the pathogenesis and natural history of hypertension. The relationship between elevated uric acid and hypertension has been proven in both animals and humans, and its relevance is already evident in childhood and adolescent population. The mechanism responsible for blood pressure increase in hyperuricemic subjects is implicating both oxidative stress and intracellular urate activity with a primary involvement of XOR (xanthine-oxidoreductase activity). An increase in the relative risk of hypertension has been confirmed by genetic data and by large meta-analyses of epidemiological data. The effects of urate-lowering treatment on blood pressure control in patients with elevated serum uric acid has been investigated in a small number of reliable studies with a large heterogeneity of patient populations and study designs. However, 2 large meta-analyses suggest a significant effect of urate-lowering treatment on blood pressure, thus confirming the significant relationship between high serum urate and blood pressure. The future research should be focused on a more appropriate identification of patients with cardiovascular hyperuricemia by considering the correct cardiovascular threshold of serum urate, the time-course of uricemia fluctuations, and the identification of reliable markers of urate overproduction that could significantly clarify the clinical and therapeutic implications of the interaction between serum uric acid and hypertension.

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尿酸和高血压：心血管风险管理的证据和未来前景回顾

尿酸是嘌呤代谢的最终产物，其升高的血清水平直接参与了高血压的发病机制和自然病程。升高的尿酸与高血压之间的关系已在动物和人类中得到证实，其相关性在儿童和青少年人群中已经很明显。导致高尿酸血症受试者血压升高的机制涉及氧化应激和细胞内尿酸盐活性，主要涉及 XOR（黄嘌呤氧化还原酶活性）。遗传数据和流行病学数据的大型荟萃分析证实了高血压相对风险的增加。已经在少数可靠的研究中调查了降尿酸治疗对血清尿酸升高患者血压控制的影响，这些研究具有很大的患者群体和研究设计的异质性。然而，两项大型荟萃分析表明降尿酸治疗对血压有显着影响，从而证实了高血清尿酸与血压之间的显着关系。未来的研究应侧重于通过考虑血清尿酸的正确心血管阈值、尿酸波动的时程、