Division of Nephrology, Department of Pediatrics, University of Alabama at Birmingham, 1600 7th Avenue South, Birmingham, AL 35233, USA.
J Clin Hypertens (Greenwich). 2012 Jun;14(6):346-52. doi: 10.1111/j.1751-7176.2012.00662.x. Epub 2012 May 21.
Uric acid has been suspected to be a risk factor for hypertension since the 1870s. Numerous epidemiological studies demonstrate an association between uric acid and both incident and prevalent hypertension in diverse populations. Studies in elderly patients have had more variable results, raising the possibility that uric acid may be more significant to hypertension in the young. Animal models support a two-phase mechanism for the development of hyperuricemic hypertension. Initially, uric acid induces vasoconstriction by activation of the renin-angiotensin system and reduction of circulating nitric oxide, which can be reversed by lowering uric acid. Over time, uric acid uptake into vascular smooth muscle cells causes cellular proliferation and secondary arteriolosclerosis that impairs pressure natriuresis, causing sodium-sensitive hypertension. Consistent with the animal model data, small clinical trials performed in adolescents with newly diagnosed essential hypertension demonstrate that at least in certain young patients, reduction of serum uric acid can mitigate blood pressure elevation. While more research is clearly necessary, the available data suggest that uric acid is likely causative in some cases of early-onset hypertension.
尿酸自 19 世纪 70 年代以来一直被怀疑是高血压的一个危险因素。大量的流行病学研究表明尿酸与不同人群的原发性和高血压性高血压之间存在关联。老年患者的研究结果则更加多变，这表明尿酸可能对年轻人的高血压更有意义。动物模型支持高尿酸血症性高血压的两阶段机制。最初，尿酸通过激活肾素-血管紧张素系统和减少循环中的一氧化氮引起血管收缩，降低尿酸可以逆转这种情况。随着时间的推移，尿酸进入血管平滑肌细胞导致细胞增殖和继发性小动脉硬化，损害压力利钠作用，导致钠敏感型高血压。与动物模型数据一致，在新诊断为原发性高血压的青少年中进行的小型临床试验表明，至少在某些年轻患者中，降低血清尿酸可以减轻血压升高。虽然显然需要更多的研究，但现有数据表明，尿酸可能在某些情况下导致早期高血压。
