血管紧张素Ⅱ和转移生长因子β1在二肾一夹高血压大鼠血管重构中的作用

目的　探讨二肾一夹高血压大鼠 ( 2 K1Ca- HR)血管重构中 Ang 、TGFβ1的作用机制。方法　动物分为实验组、对照组、治疗组 ,观察循环、组织 Ang 含量、肠系膜阻力动脉 TGFβ1 表达及对 enalapril的反应。结果　术后 2周实验组血管 Ang 明显增高 ( P<0 .0 1)持续至 12周 ,血浆 Ang 也显著升高并持续至 8周 ,但呈下降趋势 ,术后12周与术后 2周发生显著差异 ( P<0 .0 1)。实验组从 2周开始出现血管重构以后进行性加重。对照组血管组织无TGFβ1 表达 ,实验组各时相点肠系膜阻力动脉中层 VSMCs TGFβ1 表达阳性。 enalapril可降低循环、血管 Ang 至对照组水平 ,治疗组无血管形态改变 TGFβ1 表达阴性。结论　 TGFβ1 在 2 K 1C- HR血管重构中发挥作用 ,其表达活化与血管组织 Ang 的升高关系密切。enalapril具防止血管重构的血管保护作用 ,可能与其抑制了 Ang 升高、TGFβ1 表达有关

Effects of angiotensin Ⅱ and transforming growth factor beta-1 in 2k1C-HR vascular remodeling

Objective To investgate the effects of angiotensin II and TGFβ1 in 2K1C-HR vascular remodeling. Methods Rats were separated into control group, experimental group and enalapril treated group. Plasma and tissue AngⅡ were quantified by radioimmunoassy methods.TGFβ1expression was measured by immunohistochemistry. Results Plasma AngⅡ was elevated but gradually decreased to the baseline.Tissue AngⅡelevated and kept stable. Vascular remodeling appeared in 2K1C-HR. TGFβ1 expression was positive in VSMCs of 2K1C-HR mesenteric artery. Rats in therapy group were no TGFβ1 expressions. Conclusion Typical vascular remodeling is observed in 2K1C-HR.Tissue AngⅡelevated is an important factor to keep long time stable hypertension and vascular remodeling. TGFβ1 is activated by AngⅡ and participates in modulating VSMCs growth.