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目的:探讨儿童肥胖引起高血压的机制。方法:测定104例12～16岁中学儿童的血脂、胰岛素水平,Na~+K~+ATP酶和Ca~(2+)-ATP酶活性。结果:在正常血压肥胖组(ONT)和高血压肥胖组(OHT),空腹胰岛素(Ins)显著升高,而Na~+-K~+-ATP酶和Ca~(2+)-ATP酶活性显著下降,三者在ONT和OHT组之间也有显著性差异;在OHT组Ins升高,两酶活性下降。Pearson相关和多元回归分析显示,在OHT组,Ins和Ca~(2+)-ATP酶与收缩压(SBP)显著相关,Na~+-K~+-ATP酶与舒张压(DBP)显著相关。结论:高胰岛素血症、Na~+-K~+-ATP酶和Ca~(2+)-ATP酶活性降低可能在肥胖儿童高血压的发病机制中起重要作用。
Objective: To explore the mechanism of hypertension caused by obesity in children. Methods: The levels of serum lipids, insulin, Na ~ + K ~ + ATPase and Ca ~ (2 +) - ATPase in 104 children aged 12 ~ 16 years were measured. Results: Fasting insulin (Ins) increased significantly in normal blood pressure obese group (ONT) and hypertensive obesity group (OHT), while Na ~ + -K ~ + -ATPase and Ca ~ (2 +) - ATPase activity Significantly decreased. There was also a significant difference among the three groups in ONT and OHT groups. Ins increased in OHT group and the activity of both enzymes decreased. Pearson correlation and multiple regression analysis showed that there was a significant correlation between Ins and Ca ~ (2 +) - ATPase and systolic blood pressure (SBP) in OHT group, and Na ~ + -K ~ + -ATPase was significantly correlated with DBP . CONCLUSION: The decrease of hyperinsulinemia, Na ~ + -K ~ + -ATPase and Ca ~ (2 +) - ATPase activity may play an important role in the pathogenesis of hypertension in obese children.