摘要
目的低度炎症反应可能与高血压病的发生有关,血管紧张素II可能起一定作用。笔者以前的研究发现,高血压病人外周血单个核细胞白介素-1β的分泌较正常血压者升高。了解血管紧张素II在高血压病炎症反应中的作用,以及缬沙坦在高血压病中的抗炎作用,探讨高血压病的炎症反应的可能机制。方法选取24例无并发症的高血压病患者,随机分为二组,A组采用常规降压治疗(非血管紧张素转换酶抑制剂和血管紧张素II受体拮抗剂),B组使用血管紧张素II受体拮抗剂缬沙坦(代文80mg/d)治疗。分离培养外周血单个核细胞,检测细胞培养上清白介素-1β的浓度,2周后复查。外周血单个核细胞用密度梯度离心法分离培养。白介素-1β的浓度采用酶联免疫吸附法(ELISA)检测。结果缬沙坦治疗2周后,高血压病患者脂多糖刺激的外周血单个核细胞白介素-1β的分泌下降[(2857±643)pg/mL比(2146±508)pg/mL,P<0.05]。结论本研究表明高血管紧张素II可能与血压病患者外周血单个核细胞的激活状态有一定的关系。缬沙坦治疗能部分逆转高血压病的炎症反应,且与血压的降低无直接关系。
[Objective] Chronic low-grade inflammation response may contribute to the pathology of essential hypertension. Angiotensin Ⅱ（Ang Ⅱ） may be partly responsible for this process. Ang Ⅱ receptor blocker valsartan hase been reported to have anti-inflammatory effects. Our early studies showed that individuals with essential hypertension have increased interleukin-1β（IL-1β） secretion in peripherral blood mononuelear cells （PBMCs）. In this study, We study whether treatment with valsartan lowered Ⅱ-1βsecretion by PBMCs in patients with essential hypertension.[Methods] The patients（n=24） with essential hypertension （EH） were randomized to treatment with valsartan （80 mg/day, Group B） or matching routine therapy group（Group A） for 2 weeks. PBMCs were isolated by gradient centrifugation from 24 individuals. Ⅱ-1βconcentrations in supernatant from PBMCs were measured by Enzyme-linked immunosorbent assay（ELISA）. [Results] Compared with routine therapy group, patients treated with valsartan had decreased secretion of Ⅱ-1β in PBMCs after stimulated by lipopolysaccharide [（2857±643） pg/mL vs.（2146±508） pg/mL,P〈0.05）. [Conclusions] Our study suggests that Ang Ⅱ may be partly responsible for the low-grade inflammatory state of hypertension and that treatment with valsartan has anti-inflammatory effects in this condition.
出处
《中国现代医学杂志》
CAS
CSCD
北大核心
2005年第14期2214-2216,2219,共4页
China Journal of Modern Medicine
关键词
高血压病
炎症
白介素-1Β
外周血单个核细胞
缬沙坦
essential hypertension
inflammation
interleukin-1β
peripheral blood mononuclear cells
valsartan
