CAJ | 학술논문

目的:观察氯沙坦治疗对自发性高血压大鼠(SHR)主动脉重构及p22phox表达的影响.方法:36只12周龄SHR连续灌胃给予氯沙坦,剂量分别为0,15,30 mg/(kg·d),每组12只;另取12只WKY大鼠作为非高血压对照组.每周测定尾动脉压.8周后检测主动脉病理结构、血浆过氧化氢(H2O2)水平、过氧化氢酶 (CAT)活力、血浆血管紧张素Ⅱ(Ang Ⅱ)水平、主动脉p22phox的表达.结果:SHR主动脉血管壁明显增厚,尾动脉压、血浆H2O2和AngⅡ水平及主动脉p22phox的表达均显著增高,而血浆CAT活力明显下降;应用氯沙坦治疗在降低血压的同时,可改善SHRL主动脉结构,降低血浆H2O2水平和主动脉p22phox的表达,升高血浆AngⅡ水平及和CAT活力.结论: SHR主动脉血管重构涉及氧化应激,氯沙坦可改善血管重构,其机制与下调p22phox表达、抑制氧化应激有关.
목적:관찰록사탄치료대자발성고혈압대서(SHR)주동맥중구급p22phox표체적영향.방법:36지12주령SHR련속관위급여록사탄,제량분별위0,15,30 mg/(kg·d),매조12지;령취12지WKY대서작위비고혈압대조조.매주측정미동맥압.8주후검측주동맥병리결구、혈장과양화경(H2O2)수평、과양화경매 (CAT)활력、혈장혈관긴장소Ⅱ(Ang Ⅱ)수평、주동맥p22phox적표체.결과:SHR주동맥혈관벽명현증후,미동맥압、혈장H2O2화AngⅡ수평급주동맥p22phox적표체균현저증고,이혈장CAT활력명현하강;응용록사탄치료재강저혈압적동시,가개선SHRL주동맥결구,강저혈장H2O2수평화주동맥p22phox적표체,승고혈장AngⅡ수평급화CAT활력.결론: SHR주동맥혈관중구섭급양화응격,록사탄가개선혈관중구,기궤제여하조p22phox표체、억제양화응격유관.
Objective To determine the effect of losartan on vascular remodeling and the underlying mechanism in spontaneously hypertensive rats(SHR). Methods SHR of 12 weeks old were given losartan orally [0,15,30 mg/(kg·d),n=12]. The tail arterial pressure was measured every week.Eight weeks later, the pathological changes and p22phox expression in the thoracic aorta, the activity of catalase (CAT), the contents of H2O2 and AngⅡ in the plasma were evaluated. Results Blood pressure was increased in the SHR accompanied by the thickened wall and increased p22phox expression in the thoracic aorta. The plasma levels of H2O2 and AngⅡwere elevated while the CAT level was decreased in the SHR. Administration of losartan reversed the thickened wall and increased the CAT activity concomitantly with the decreased plasma levels of H2O2 and p22phox expression in the SHR. The plasma level of AngⅡincreased after the losartan treatment. Conclusion Oxidative stress induces the vascular remodeling of the aorta in the SHR. Losartan can reverse the vascular remodeling through down-regulating p22phox expression and inhibiting the oxidative stress.