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目的:观察波生坦和硝苯地平对脱氧皮质酮(DOCA)-盐敏感高血压鼠(DHR)血压、主动脉结构、血浆内皮素-1(ET-1)和主动脉组织ET-1 mRNA表达的影响,探讨其可能的作用及其机制。方法:40只SD大鼠, 等分为正常对照组、DHR对照组、波生坦组和硝苯地平组,波生坦组给予波生坦100 mg·kg-1·d-1灌胃,硝苯地平组给予35 mg·kg-1·d-1灌胃,每周测尾动脉血压1次,4周后处死,抽取动脉血放射免疫法测血浆ET-1 浓度,取主动脉分别作病理分析和逆转录聚合酶链反应检测ET-1 mRNA表达。结果:DHR对照组血压明显升高,血管平滑肌细胞肥大,弹力纤维层增厚,中层厚度及中层厚度／内径明显增大。波生坦组血压上升幅度降低, 上述血管组织变化明显改善。硝苯地平可抑制DHR血压上升,血管组织变化与模型对照组相似。血浆ET-1浓度在DHR对照组、波生坦组和硝苯地平组均有显著升高,但以波生坦组升高更为显著;DHR对照组、波生坦组和硝苯地平组主动脉组织ET-1 mRNA表达与正常对照组相比,均有显著增加,但3组间差异无统计学意义。结论:波生坦可降低DHR上升的血压,改善主动脉重塑可能系波生坦阻断了ET-1与其受体结合的结果。硝苯地平能抑制DHR的血压升高,但不能改善主动脉的重塑。
OBJECTIVE: To observe the effects of bosentan and nifedipine on blood pressure, the structure of aorta, plasma endothelin-1 (ET-1) and ET-1 mRNA in aortal tissue of DOCA-salt-sensitive hypertensive rats Expression of the impact of its possible role and its mechanism. Methods: Forty SD rats were equally divided into normal control group, DHR control group, bosentan group and nifedipine group. Bosentan group was given Bosentan 100 mg · kg -1 · d -1 intragastrically, Nifedipine group was given 35 mg · kg-1 · d-1 gavage, tail artery blood pressure was measured once a week, 4 weeks after the death, the extraction of arterial blood radioimmunoassay plasma ET-1 concentration, take the aorta were Pathological analysis and reverse transcription polymerase chain reaction detection of ET-1 mRNA expression. Results: In DHR control group, blood pressure was significantly increased, vascular smooth muscle cells hypertrophy, elastic fiber layer thickening, middle thickness and middle thickness / diameter increased significantly. Bosentan group decreased blood pressure, vascular changes significantly improved. Nifedipine can inhibit the increase of DHR blood pressure, vascular tissue changes and model control group similar. Plasma ET-1 levels in DHR control group, bosentan group and nifedipine group were significantly increased, but the Bosentan group increased more significantly; DHR control group, bosentan group and nifedipine group Compared with the normal control group, the ET-1 mRNA expression in aorta increased significantly, but there was no significant difference among the three groups. CONCLUSION: Bosentan can reduce the rise of DHR blood pressure and improve aortic remodeling. Bosentan blocked the binding of ET-1 to its receptor. Nifedipine can inhibit DHR blood pressure, but can not improve aortic remodeling.