肾性高血压血管重构中血红素加氧酶的作用  

Effect of heme oxygenase on vascular remodeling in renal hypertension

作　　者：韩莉[1] 庞东卫[2] 马铁民[1] 徐海[1] 吴立玲[1] 

机构地区：[1]北京大学医学部病理生理教研室,北京100083 [2]包头医学院生理学教研室,内蒙古包头014010

出　　处：《中国病理生理杂志》2005年第3期427-431,共5页Chinese Journal of Pathophysiology

摘　　要：目的 :研究血红素加氧酶 (HO)在肾性高血压所致的血管重构中的作用。方法 :采用两肾一夹(2K1C)肾性高血压大鼠模型 ,测定术后 4周主动脉中膜的厚度、主动脉组织HO活性及HO - 1蛋白表达水平。结果 :① 2K1C肾性高血压大鼠术后 2周开始出现高血压 ,在术后 4周血压稳定升高 ;Hemin组术后 4周未见血压升高。②术后 4周 2K1C组大鼠可见主动脉中膜的厚度较假手术组高 2 7 5 % (P <0 0 1) ;Hemin组主动脉中膜的厚度较 2K1C组低 16 1% (P <0 0 1)。③术后 4周 2K1C组主动脉组织HO - 1蛋白表达量明显高于假手术组 (P <0 0 1) ;HO酶活性高于假手术组 (P <0 0 5 )。结论 :肾性高血压导致血管重构的过程中HO系统激活。诱导HO可以降低肾性高血压大鼠的血压 ,抑制主动脉中膜平滑肌层的增厚。AIM: To investigate the effect of heme oxygenase on vascular remodeling in renal hypertension. METHODS: Male Wistar rats were randomly divided into sham-operated, 2K1C (two-kidney one-clip) and hemin-induced groups. Four weeks after the treatments, the thickness of aortic media and HO enzymatic activity of the aorta were determined. Immunohistochemical staining was carried out to detect protein of HO-1 in the aorta. RESULTS: The blood pressure in 2K1C renal hypertension rats started to increase two weeks after the surgery and stabled at a high level at the 4th week. Hemin, an inducer of HO-1, markedly inhibited the increase in blood pressure. Aortic medium thickness of the 2K1C rats at 4th week was 27 5% thicker than that in the sham-operated rats. The thickness of aortic medium of the hemin-induced rats was 16 1% less than that in 2K1C group. At the 4th week after operation, protein level and enzymatic activity of HO-1 in aorta were higher than that in 2K1C group compared to those in the sham-operated group. CONCLUSION: Renal hypertension caused vascular remodeling and the activation of HO-1. HO-1 induction decreased the blood pressure of renal hypertension and reduced vascular remodeling.

关 键 词：血红素氧化酶(脱环) 高血压 肾性 血管紧张素Ⅱ 血管重建 

分 类 号：R363[医药卫生—病理学]