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目的 :评价卡托普利对肾实质性高血压 (RPH)大鼠肾实质的保护作用 ,并探讨其对RPH大鼠内皮由来因子的调控作用。方法 :通过大鼠肾次全切除加高盐喂养法制备RPH动物模型 ,研究卡托普利对残余肾组织、超微结构的病理改变 ,并通过免疫组化RT -PCR法检测两种内皮由来因子 (cNOS、ET - 1)的分布及表达。结果 :卡托普利降压作用与空白对照组比较均有统计学差异 (P <0 .0 5 ) ,可减轻肾脏病理改变 ,对肾脏局部ETmRNAs表达呈抑制并对cNOS表达上调。结论 :卡托普利可能是通过对肾脏局部ET - 1mRNA表达、分泌的抑制和cNOSmRNA表达、分泌的上调两条途径来实现其降压 ,保护肾功能的作用
Objective: To evaluate the protective effect of captopril on renal parenchyma in rats with renal parenchymal hypertension (RPH) and to explore its regulatory effect on the endothelial factor in RPH rats. Methods: RPH animal model was established by sub-total nephrectomy and high-salt diet in rats. The histopathological changes of residual renal tissue and ultrastructure were observed by Captopril. The two endothelial cells were detected by immunohistochemical RT-PCR Distribution and expression of cNOS and ET - 1. Results: The antihypertensive effects of captopril were significantly different from those of the blank control group (P <0.05). The antihypertensive effect of captopril decreased the renal pathological changes and inhibited the expression of ETmRNAs and up-regulated cNOS in the kidney. Conclusions: Captopril may be able to achieve its antihypertensive effect and renal function protection by inhibiting the expression and secretion of ET - 1 mRNA and the up - regulation of cNOS mRNA expression and secretion