高血压血清生长因子与血管紧张素Ⅱ的相关性及对早期肾功能的影响

Correlationship of serum growth factors and plasma angiotensin Ⅱ and it's effects on microalbuminuria in hypertensives

目的探讨原发性高血压(EH)患者血清转化生长因子β(TGF-β)、血小板源性生长因子(PDGF)、胰岛素样生长因子-Ⅰ(IGF-Ⅰ)与血浆血管紧张素Ⅱ(AngⅡ)水平的相关性及其对早期肾功能损害的影响。方法用放射免疫法(RIA)检测28例健康者(对照组)血清PDGF、血清IGF-Ⅰ、血浆AngⅡ和66例EH患者血清PDGF、血清IGF-Ⅰ、血浆AngⅡ及早晨尿微量白蛋白(mALB);同时用酶联免疫法(ELISA)测定其血清TGF-β;根据EH患者尿mALB量分为EH伴mALB异常组31例(mALB≥8.68mg/L)和EH伴mALB正常组35例(mALB<8.68mg/L)。结果与对照组比较,EH伴mALB正常组血浆AngⅡ、血清TGF-β、PDGF及IGF-Ⅰ均增高(P<0.05),EH伴mALB异常组增高显著(P<0.01);相关分析显示EH患者AngⅡ与TGF-β、PDGF及IGF-Ⅰ成正相关;mALB与AngⅡ、TGF-β成正相关,与PDGF、IGF-Ⅰ无相关性;逐步回归分析显示AngⅡ是早期肾功能损害的独立预测因素。结论血清生长因子参与原发性高血压及肾功能损害的发病机制,AngⅡ在此过程中起重要作用。

Objective To explore the relationships between plasma angiotensin Ⅱ （Ang Ⅱ ） and serum insulin-like growth factor-Ⅰ （IGF-Ⅰ）, tansforming growth factor-beta（TGF-β）, platelet-derived growth factor （PDGF） respectively and the influence of growth factors as well as Ang Ⅱ on early renal damage in patients with essential hypertension （EH）. Methods Plasma Ang Ⅱ, serum PDGF, serum IGF-Ⅰ, urinary microalbumin with radioimmunoassay methods and serum TGF-β with enzyme immunoassay method （ELISA） were measured. The subjects were categorized into two groups： 28 apparently healthy people （control group） and 66 patients with EH （EH group）. Then, the EH patients were divided into an abnormal microalbuminuria （mALB） group （31 cases） and a normal mALB group （35 cases）. Results Serum leveles of Ang Ⅱ, TGF-β, PDGF and IGF-Ⅰ in EH patients were higher than that in control group （P〈0.05）, and these changes were more obvious in abnormal mALB group than in normal mALB group （P〈0.01）. In the EH patients, serum TGF-β, PDGF and IGF-Ⅰ were associated respectively with plasma Ang Ⅱ, and mALB was associated with Ang Ⅱ and TGF-β, but not correlated to PDGF and IGF-Ⅰ levels. Stepwise regression showed that Ang Ⅱserved as was the independent risk factor for EH-indued renal damage. Conclusion Growth factors and Ang Ⅱ play very important roles in the pathogenesis of hypertension and early renal damage.