Feig Daniel I, Kang Duk-Hee, Nakagawa Takahiko, Mazzali Marilda, Johnson Richard J
Department of Pediatrics, Renal Section, MC3-2482, Baylor College of Medicine, 1102 Bates Street, Houston, TX 77030, USA.
Curr Hypertens Rep. 2006 May;8(2):111-5. doi: 10.1007/s11906-006-0005-z.
Epidemiologic studies published during the past 3 years support the possible role of uric acid in the onset of essential hypertension. Data from several large, longitudinal cardiovascular disease studies indicate that elevated serum uric acid is a predictor of incident hypertension and blood pressure progression. In a pediatric study, more than 90% of children with essential hypertension have serum uric acid levels above 5.5 mg/dL. During the same period, laboratory studies have provided compelling mechanistic evidence to explain the clinical observations. Uric acid causes hypertension in a rat model through the activation of the renin-angiotensin system, downregulation of nitric oxide, and induction of endothelial dysfunction and vascular smooth muscle proliferation. Ongoing clinical trials will elucidate the role of uric acid in human hypertension and will determine whether control of uric acid may be a new way to prevent or treat essential hypertension.
过去3年发表的流行病学研究支持尿酸在原发性高血压发病中可能发挥的作用。几项大型纵向心血管疾病研究的数据表明,血清尿酸升高是新发高血压和血压进展的预测指标。在一项儿科研究中,超过90%的原发性高血压儿童血清尿酸水平高于5.5mg/dL。同期,实验室研究提供了有力的机制证据来解释这些临床观察结果。尿酸通过激活肾素-血管紧张素系统、下调一氧化氮、诱导内皮功能障碍和血管平滑肌增殖,在大鼠模型中导致高血压。正在进行的临床试验将阐明尿酸在人类高血压中的作用,并将确定控制尿酸是否可能成为预防或治疗原发性高血压的新方法。