【摘要】 目的　观察依那普利对DOCA -盐诱导的高血压大鼠 (DHR)血压、主动脉结构、血浆内皮素 (ET 1)和主动脉组织ET 1mRNA表达的影响 ,并探讨依那普利不影响其变化的可能机制。方法　 3 0只SD大鼠 ,等分和制作为正常对照组、模型对照组、依那普利组。依那普利组给予依那普利 2 0mg·kg- 1 ·d- 1 灌胃。每周测血压一次。四周后处死 ,抽动脉血放免法测血浆ET -1浓度、肾素活性 (PRA) ,取主动脉分别作病理分析和RT -PCR检测ET 1mRNA表达。结果　模型对照组血压明显上升 ,血管平滑肌细胞 (VSMC)肥大 ,弹力纤维层增厚 ,中层厚度及中层厚度 /内径明显增大。依那普利组血压也明显上升 ,四周后仅比模型对照组低 9mmHg ,两者相比差别无统计学意义 ,主动脉亦明显重塑。血浆肾素活性 :模型对照组和依那普利组显著低于正常对照组 ;依那普利组与模型对照组相比无差别 ;血浆ET 1及ET 1mRNA表达 :模型对照组和依那普利组显著高于正常对照组 ;依那普利组与模型对照组相比无差别。结论　依那普利不能改善DHR主动脉重塑 ,可能是DHR主动脉局部肾素 -血管紧张素系统 (RAS)受到抑制 ,低水平的RAS对血管组织增殖无重要作用更多还原

【Abstract】 Objective To study the effect of enalapril on systolic blood pressure(SBP), aortic structure, plasmatic endothelin-1 (ET-1) and aortic ET-1 mRNA expression in deoxycorticosterone acetate-salt induced hypertensive rats (DHR). Methods Thirty male Sprague-Dawley rats were unilaterally nephrectomized and diverged into three groups. DOCA subcutaneously injection (50 mg·kg -1·week -1) and 1% saline drinking water were used to creat hypertension model. One of model group was given enalapril 20 mg·kg -1·d -1 (enalapril group) for 4 weeks, the other receivel placebo. Plasma ET-1 was measured by radioimmunoassay. Aortas were dissected, for histologic study. RT-PCR was used to determine the ET-1 mRNA. Results In model placebo group, SBP increased significantly.\ VSMC were hypertrophied and proliferated; media thickness (MT) and MT/LD ratio increased significantly. Enalapril was not able to inhibit the development of SBP, or ameliorat vascular remodelling. Plasma ET-1 and ET-1 mRNA expression in model control group and enalapril group were higher than that in normal control group, with no significant difference between them. Conclusoins Enalapril coud not improve vascular remodeling in DOCA-Salt induced hypertenive rats. The depressed local RAS may be attributed to the failure of developement of vascular hypertrophy and mitogenesis.更多还原