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目的通过观察慢性盐负荷及补钾后血浆脂联素水平的变化及其与动脉血压的关系,探讨脂联素在血压盐敏感性发生发展中的作用及补钾的保护意义。方法选取30例年龄在16～60岁的血压正常者参与为期3周的慢性盐负荷及补钾干预试验,包括基线调查3d,低盐饮食、高盐饮食、高盐补钾饮食各7d。根据其平均动脉压(MAP)于高盐饮食期较低盐饮食期升高幅度≥10%为标准分为盐敏感组(n=10)和盐不敏感组(n=20),分别于基线及各干预期末抽取空腹静脉血标本。血浆脂联素用酶联免疫吸附法测定。结果盐敏感检出率为33%。盐负荷后,盐敏感组血浆脂联素的浓度有所下降,但差异无统计学意义,而盐不敏感组血浆脂联素的浓度明显升高[(7.3±3.9)比(5.8±2.2)mg/L,P<0.05];在高盐摄入的基础上大剂量口服补钾可以逆转高盐负荷对盐敏感组血浆脂联素浓度的影响[(8.2±1.1)比(6.2±0.7)mg/L,P<0.05]。盐敏感组盐负荷前后及补钾前后血浆脂联素变化幅度与MAP变化幅度均呈负相关(r=-0.639,r=-0.708,均P<0.05)。结论血压盐敏感者于高盐负荷后动脉血压升高,而血浆脂联素不升高;同时补充钾盐可以逆转盐负荷诱导的血压和脂联素变化。提示补钾除拮抗钠盐的升压作用外,可能通过升高脂联素水平而发挥调节血压和心血管保护作用。
Objective To observe the effect of chronic salt stress on plasma adiponectin level and its relationship with arterial blood pressure to explore the role of adiponectin in the development of blood pressure salt sensitivity and its protective significance. Methods Thirty patients with normotensive aged 16-60 years were enrolled in the three-week chronic salt stress and potassium intervention trials, including baseline survey for 3d, low-salt diet, high-salt diet and high-salt potassium diet for 7 days. According to the average arterial pressure (MAP) of salt-sensitive group (n = 10) and salt-insensitive group (n = 20) At the end of each intervention period, fasting venous blood samples were taken. Plasma adiponectin was measured by enzyme-linked immunosorbent assay. The results of salt-sensitive detection rate of 33%. After salt loading, plasma adiponectin concentration decreased in the salt-sensitive group, but the difference was not statistically significant, but the concentration of plasma adiponectin in salt-sensitive group was significantly higher than that in salt-sensitive group [(7.3 ± 3.9) vs (5.8 ± 2.2) (8.2 ± 1.1) vs (6.2 ± 0.7) mg / L, P <0.05]. On the basis of high salt intake, high dose of oral potassium supplement could reverse the effect of high salt load on plasma adiponectin concentration in salt- mg / L, P <0.05]. The change range of plasma adiponectin before and after salt-sensitive group and before and after potassium supplementation were negatively correlated with the amplitude of MAP (r = -0.639, r = -0.708, all P <0.05). Conclusions Blood pressure and salt sensitivity increased after high salt stress, while plasma adiponectin did not increase. At the same time potassium supplementation reversed the changes of blood pressure and adiponectin induced by salt stress. Tip potassium in addition to antagonizing the role of the pressure of sodium, it may by raising the level of adiponectin play a role in regulating blood pressure and cardiovascular protection.