原发性高血压心血管重构的机制及氯沙坦的干预研究

The mechanism of cardiovascular remodeling in essential hypertensive subjects and the intervenient effects of Losartan

目的 探讨血管内皮功能失调、细胞内钙超负荷与高血压心血管重构的关系及氯沙坦的干预作用。方法 入选原发性轻中度高血压 (EH)伴左室肥厚病人 30例、正常血压 (NT)对照组 30例 ,EH组给予Losartan 5 0～ 10 0mg/d治疗 40周 ,治疗前后检测左室重量指数 (LVMI)、颈总动脉内膜中层厚 (IMT)、血管内皮依赖舒张功能、血清一氧化氮(NO)、血浆内皮素 (ET)、淋巴细胞胞浆内游离钙 ([Ca2 + ]i)等项目。结果 治疗前EH组病人IMT、血浆ET、[Ca2 + ]i均显著性增加 ,而血流介导血管舒张 (FMD)、血清NO则显著减少 ;治疗后LVMI、IMT、血浆ET、[Ca2 + ]i均显著性减少 ,而FMD、血清NO则显著性增加。结论 除肾素 -血管紧张素系统 (RAS)外 ,血管内皮功能失调与细胞内钙超负荷可能是影响高血压心血管重构的重要环节。

Objective To investigate the relationship among dysfunction of vascular endothelium, intracellular calcium over-load and cardiovascular remodeling in essential hypertensive subjects and the intervenient effects of Losartan. Methods 30 patients with essential hypertension and left ventricular hypertrophy(LVH) were treated with Losartan(50～100 mg/d) for 40 weeks. Left ventricular mass index(LVMI), carotid intima-media thicknees(IMT), endothelium-dependent flow-mediated vascular dilation(FMD), Serum Nitric Oxide(NO), Plasma Endothelin(ET), and peripheral lymphocyte cytosolic calcium([Ca 2+ ]i) were assessed before and after treatment. There were 30 persons in normotensive control group(NT).Results Compared with NT group, the IMT, plasma ET and [Ca 2+ ]i were all significantly greater but FMD and serum NO were significantly less in EH group before Losartan treatment. After Losartan treatment, LVMI, IMT, plasma ET and [Ca 2+ ]i were all significantly decreased but FMD and serum NO were significantly increased.Conclusion Besides Renin-Angiotensin system(RAS), dysfunction of vascular endothelium and intracellular calciun over-load may be all involved in the process of cardiovascular remodeling.