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目的观察慢性盐负荷对血压正常盐敏感者的血管内皮标志物的影响。方法以29例血压正常健康自愿者为研究对象,采用慢性盐负荷试验确定血压盐敏感性,观察盐敏感者和盐不敏感者在平衡饮食期、高盐饮食期及低盐饮食期的24 h动态血压、血浆vWF、血、尿一氧化氮(NO)及内皮素-1(ET-1)等血管内皮标志物的变化,综合评价慢性盐负荷对血压正常盐敏感者血管内皮标志物的影响。结果29例血压正常健康自愿者中,检出盐敏感者(SS)11例(37.9%),盐不敏感者(SR)18例;SS组的昼夜平均动脉压差值较SR组显著缩小,高盐负荷后血压显著升高;高盐饮食后,SS组血浆vWF水平显著升高,血、尿NO含量显著减少,而SR组在盐负荷前后变化不著;血浆ET-1在盐负荷前后SS组与SR组之间比较无显著差异。结论部分血压正常个体表现为血压盐敏感性且存在显著的血压昼夜节律性改变;血压正常盐敏感者在高盐负荷时血浆vWF显著升高而血、尿NO含量显著减少,提示血压正常盐敏感者存在高盐介导的血管内皮功能异常。
Objective To observe the effects of chronic salt stress on vascular endothelial markers in patients with normotensive salt. Methods Twenty-nine patients with normal blood pressure were selected as the research object. The chronic salt stress test was used to determine the blood pressure-sensitiveness. The salt-sensitive and salt-insensitive subjects were observed at 24 h after balanced diet, high salt diet and low salt diet The changes of vascular endothelial markers such as ambulatory blood pressure, plasma vWF, blood, urinary nitric oxide (NO) and endothelin-1 (ET-1) were evaluated comprehensively to evaluate the effects of chronic salt stress on the vascular endothelial markers . Results Among 29 healthy volunteers with normal blood pressure, 11 (37.9%) patients with salt sensitivity (SS) and 18 patients with salt insensitivity (SR) were detected. The mean arterial pressure difference between day and night in SS group was significantly lower than that in SR group After high-salt stress, blood pressure increased significantly. After high-salt diet, plasma vWF level in SS group was significantly increased, NO in blood and urine was significantly decreased, while SR group did not change before and after salt loading. Plasma ET- There was no significant difference between SS group and SR group. Conclusions Some individuals with normotension show blood pressure-sensitivity and circadian rhythm of blood pressure. The plasma vWF levels are significantly increased in patients with normotensive salt-sensitive and the levels of NO and NO in blood and urine are significantly decreased, indicating that normotensive salt-sensitive There is a high salt-mediated endothelial dysfunction.