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目的研究血管紧张素Ⅱ受体-1阻断剂氯沙坦对肾性高血压大鼠血管重塑及其分裂原激活的蛋白激酶p38MAPK表达的影响。方法两肾一夹法复制肾血管性高血压大鼠(2K1C-RHR)模型;采用尾动脉套管法和颈动脉插管法测量大鼠血压,大血管(胸主动脉)苏木素-伊红(HE)染色进行形态学观察;治疗组采用氯沙坦灌胃治疗;反转录-聚合酶链反应和免疫印迹方法检测主动脉血管p38MAPK的表达。结果实验组大鼠和对照组(假手术组)普通饲料饲养6周,模型组血压为(158±7)mmHg,对照组血压为(104±11)mmHg;两组间差异有显著性(P<0.05);模型组大鼠胸主动脉内径增大,中层厚度增大,细胞层数略微增加。经氯沙坦治疗后,血压降为(132±9)mmHg,血管重塑现象氯沙坦治疗组较实验组明显改善;免疫印迹方法检测,重塑血管主动脉血管p38MAPK的表达增高,氯沙坦干预可以抑制其表达。结论氯沙坦可明显改善肾血管性高血压大鼠血管重塑,这种调节可能是通过阻断血管紧张素Ⅱ受体信号途径或调节p38MAPK表达而发挥作用。
Objective To investigate the effects of losartan, an angiotensin Ⅱ receptor antagonist, on vascular remodeling and p38MAPK expression in mitogen - activated protein kinase (reno) in renovascular hypertensive rats. Methods The model of renal hypertensive rats (2K1C-RHR) was duplicated by two kidneys and one clamp. The blood pressure, blood vessels (thoracic aorta) hematoxylin and eosin (HEK) were measured by tail artery catheterization and carotid artery cannulation. HE staining and morphological observation. The treatment group was treated with losartan intragastrically. The expression of p38MAPK in aortas was detected by reverse transcription polymerase chain reaction (RT-PCR) and Western blotting. Results The rats in the experimental group and the control group (sham operation group) were fed with normal diet for 6 weeks. The blood pressure was 158 ± 7 mmHg in the model group and 104 ± 11 mmHg in the control group. The difference between the two groups was significant <0.05). The diameter of thoracic aorta in model group increased, the thickness of middle layer increased, and the number of cell layers increased slightly. After treatment with losartan, the blood pressure drop was (132 ± 9) mmHg, and the remodeling of losartan group was significantly improved compared with the experimental group. The expression of p38MAPK in remodeled vascular aorta was increased by immunoblotting, Tan intervention can inhibit its expression. Conclusion Losartan can significantly improve vascular remodeling in renovascular hypertensive rats. This regulation may play a role by blocking the signal pathway of angiotensin Ⅱ receptor or regulating the expression of p38MAPK.