原发性高血压患者血浆 ghrelin水平的改变及其影响因素

 【目的】研究原发性高血压患者血浆生长激素促分泌素受体(GHSR)的内源性配体 ghrelin水平的改变及抗高血压药物治疗对血浆ghrelin水平的影响。【方法】 入选41 例健康志愿者作为对照组,37 例原发性高血压患者并实施降压治疗,采用酶联免疫法测定健康对照组和原发性高血压患者治疗前后血浆 ghrelin水平及其它内皮相关指标,并分析血浆ghrelin与血压(BP)、体质量指数( BMI)、腰围、腰臀比、血脂、空腹血糖、同型半胱氨酸(Hcy)、内皮素(ET-1)、NO、vWF之间的关系。【结果】 原发性高血压患者血浆ghrelin水平较健康对照组明显升高(P < 0.01),而血浆Hcy、NO水平与对照组比较无明显差异(P > 0.05)。该组经降压治疗9个月后患者BP、BMI、血脂及血浆ghrelin、ET-1、vWF水平均降低(P < 0.01),且血浆Hcy、NO水平无显著变化(P > 0.05)。相关性分析表明血浆ghrelin水平与ET-1呈显著正相关(r = 0.37,P < 0.01),而与血糖、BMI呈负相关(r = -0.29,P < 0.01;r = -0.26,P < 0.05)。多元线性逐步回归分析提示ET-1是影响血浆 ghrelin水平的独立相关因素。【结论】 高血压患者血浆ghrelin水平的显著升高可能与高血压患者血浆中高水平的ET-1刺激了机体自身的ghrelin的代偿分泌有关。

Changes of Plasma Ghrelin Levels and Relevant Factors in Essential Hypertensive Patients

【Objective】 This study aimed to measure the changed plasma ghrelin levels and relevant factors in hypertensive people before and after blood pressure control treatment. 【Methods】 Thirty-seven hypertensive patients and 41 healthy volunteers were selected. The plasma ghrelin level was determined by ELISA and its association with clinical characteristics such as blood pressure (BP) and endothelial related indices such as Hcy, ET-1, NO, and vWF were evaluated. 【Results】 Plasma ghrelin levels were significantly elevated in hypertensive patients compared to healthy controls, while plasma Hcy and NO levels were not show statistic significance between two groups. After treatment on BP control for 9 months, BP, BMI, and plasma levels of blood lipid, ghrelin, ET-1,and vWF were all significantly decreased(P < 0.01) in hypertensive patients, while plasma Hcy and NO levels were not significantly changed (P > 0.05). Plasma ghrelin levels correlated positively with ET-1 levels (r = 0.37,P < 0.01), and correlated inversely with both BMI and fasting plasma glucose (r = -0.29,P < 0.01;r = -0.26,P < 0.05). In a multiple regression analysis, using ghrelin as a dependent variable, the plasma ET-1 level was significant independent variables. 【Conclusions】 This study indicates the elevation of plasma ghrelin level during the pathogenesis of hypertension probably is a protective compensatory response, which can resist the increased circulating ET-1 levels.