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引用次数: 0
摘要
调查高尿酸血症与高血压之间的关系是高血压研究中一个引人入胜的领域。嘌呤代谢的最终产物是尿酸(UA),血清尿酸(SUA)水平的升高直接导致高血压的发生。大量研究证实,高尿酸血症是高血压的重要危险因素。此外,初步临床试验表明,旨在降低 SUA 水平的治疗干预措施可降低因高尿酸血症导致的高血压患者的血压(BP)。最新研究表明,高尿酸血症可通过多种机制促进高血压的发生,包括氧化应激、炎症、一氧化氮(NO)合成减少、活性氧(ROS)激活、胰岛素抵抗、血管平滑肌增生和肾功能损害。鉴于高尿酸血症和高血压之间的相互联系,找出潜在的治疗方法以便及时干预,从而阻止高尿酸血症患者的高血压进展,是非常有利的。本文回顾了有关高尿酸血症诱发高血压发病机制的研究进展。
The relationship between hyperuricemia and hypertension: a short review of current evidence
The investigation of the relationship between hyperuricemia and hypertension is a captivating field in hypertension research. The final product of purine metabolism is uric acid (UA), and the elevation of serum UA (SUA) levels directly contributes to the development of hypertension. Numerous studies have substantiated that hyperuricemia is a significant risk factor for hypertension. Furthermore, initial clinical trials have demonstrated that therapeutic interventions aimed at reducing SUA levels lower blood pressure (BP) in individuals with hypertension attributed to hyperuricemia. Recent research has demonstrated that hyperuricemia can facilitate the onset of hypertension via multiple mechanisms, including oxidative stress, inflammation, diminished nitric oxide (NO) synthesis, activation of reactive oxygen species (ROS), insulin resistance, vascular smooth muscle proliferation, and renal impairment. Given the interconnectedness between hyperuricemia and hypertension, it is advantageous to identify potential therapeutic approaches for timely intervention in order to impede the advancement of hypertension in individuals with hyperuricemia. This article reviews the research progress on the pathogenesis of hyperuricemia-induced hypertension.