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目的通过慢性盐负荷及补钾试验,探索其对盐敏感者氧化应激和内皮功能的影响,探讨盐敏感高血压有效的预防措施。方法在陕西农村选择正常血压或1级高血压患者60人,进行基线调查和饮食干预研究。每个阶段的第2天和最后3 d测量体重和血压。测定各阶段尿钠、钾排泄量、血浆一氧化氮、丙二醛、尿一氧化氮含量,采用t检验统计学处理。结果无论盐敏感者还是盐不敏感者,低盐比基线血、尿一氧化氮升高,丙二醛、24 h尿微量清蛋白降低差异有统计学意义(P<0.05或P<0.01);高盐比低盐血、尿一氧化氮降低,丙二醛降低,差异有统计学意义(P<0.05或P<0.01);高盐比低盐血、尿一氧化氮降低,丙二醛升高(P<0.05或P<0.01);补钾后血、尿一氧化氮升高,丙二醛、24 h尿微量清蛋白降低,且盐敏感者比盐不敏感者变化更为显著。结论氧化应激在盐敏感者内皮功能损害中起着重要的作用。补钾具有保护作用,可改善高盐引起的肾脏损害。
Objective To investigate the effects of chronic salt stress and potassium supplementation on oxidative stress and endothelial function in salt-sensitive patients and to explore effective preventive measures for salt-sensitive hypertension. Methods Sixty patients with normotensive or grade 1 hypertension in rural areas of Shaanxi Province were selected for baseline investigation and diet intervention study. Body weight and blood pressure were measured on the second day and the last 3 days of each phase. Urine sodium and potassium excretion, plasma nitric oxide, malondialdehyde and urinary nitric oxide were measured at each stage, and were analyzed by t-test. Results Low salinity was significantly higher than baseline blood and urine nitric oxide, malondialdehyde and 24 h urine microalbumin in both salt sensitive and salt insensitive groups (P <0.05 or P <0.01). High salt than low salt blood, urine nitric oxide decreased, malondialdehyde decreased, the difference was statistically significant (P <0.05 or P <0.01); high salt than low salt blood, urine nitric oxide decreased, (P <0.05 or P <0.01). After potassium supplementation, serum nitric oxide and nitric oxide levels in serum and urine malondialdehyde and 24 h urine microalbumin decreased, and salt sensitivity was more significant than salt insensitivity. Conclusion Oxidative stress plays an important role in endothelial dysfunction in salt sensitive patients. Potassium has a protective effect, can improve kidney damage caused by high salt.