目的:探讨阿托伐他汀控制自发性高血压大鼠(SHR)高血压的机制,研究阿托伐他汀对SHR血浆内皮素-1(ET-1)和主动脉一氧化氮合酶(NOS)的影响,以及对SHR的主动脉平滑肌细胞(ASMC)凋亡和P27蛋白表达的影响。方法:选用8周龄SHR 12只,随机分为...目的:探讨阿托伐他汀控制自发性高血压大鼠(SHR)高血压的机制,研究阿托伐他汀对SHR血浆内皮素-1(ET-1)和主动脉一氧化氮合酶(NOS)的影响,以及对SHR的主动脉平滑肌细胞(ASMC)凋亡和P27蛋白表达的影响。方法:选用8周龄SHR 12只,随机分为阿托伐他汀治疗组(ATV组,N=6)和SHR组(N=6),并以同周龄 WKY(N=6)作为对照。ATV组给以阿托伐他汀(50MG·KG-1·D-1)灌胃。10周后观察3组大鼠血压、血清总胆固醇 (TC)、总甘油三酯(TG)含量变化,血浆ET-1和主动脉NOS活性的改变,以及TUNEL法检测ASMC凋亡率,测定动脉 ASMC P27蛋白表达。结果:阿托伐他汀给药10周后,ATV组动脉收缩压显著低于SHR组[(134．17±3．60)MMHG VS (173．33±3．78)MMHG,P<0．01];ATV组血清TC和TG浓度均显著低于SHR组(P<0．01,P<0．01)。同时,阿托伐他汀显著降低SHR血浆ET-1水平[(130．04±40．07)NG/L VS(196．74±59．69)NG/L,P<0．05]和增加SHR主动脉NOS 活性[(0．189±0．040)KU/G PROTEIN VS (0．124±0．057)KU／G PROTEIN,P<0．01];ATV组ASMC凋亡率显著高于SHR组 (16．94％±3．08％ VS 9．01％±2．36％,P<0．01);ATV组ASMC P27蛋白表达阳性率显著高于WKY大鼠(33．02％± 5．01％ VS 24．25％±4．41％,P<0．05),而SHR组该指标明显低于WKY大鼠(16．08％±7．09％ VS 24．25％±4．41％, P<0．05)。结论:阿托伐他汀控制SHR血压增高,其机制可能与降低SHR的血浆ET-1水平和增高主动脉NOS活性,以及增高ASMC凋亡率和P27蛋白表达阳性率有关。展开更多
Objective:To investigate the changes of calcium transport protein activities of aortic vascular smooth muscle cell in the progress of hypertension,evaluate the effects of irbesartan on them,then to elucidate the relat...Objective:To investigate the changes of calcium transport protein activities of aortic vascular smooth muscle cell in the progress of hypertension,evaluate the effects of irbesartan on them,then to elucidate the relationship between cell calcium transport protein and hypertension.Methods:Sixteen sixteen-week-old SHR were randomized into irbesartan treated group(IBT group,n=8)and distilled water group(DW group,n=8),and Wistar-Kyoto rats(WKY)as normal controls.Irbesartan and appropriate amounts of distilled water were administered respectively for 14 weeks by gavage.Blood pressure of caudal artery was examined before and after treatment,activities of Na+-K+-ATPase and Ca 2+-Mg 2+-ATPase of thoracic vascular aorta smooth muscle cell were measured.Results:Blood pressure in IBT group was much lower than that in DW group(129.17±3.71)vs(186.50±6.06),P<0.01).Compared with DW group,activities of Na+-K+-ATPase and Ca 2+-Mg 2+-ATPase of thoracic vascular aorta smooth muscle cell were remarkedly higher in both IBT group and WKY group(5.56±0.92)vs(2.91±0.56),P<0.01;(4.83±0.86)vs(2.76±0.43),P<0.01),(5.98±0.63)vs(2.91±0.56),P<0.01;(4.94±0.84)vs(2.76±0.43),P<0.01),while there was a slight difference between IBT group and WKY group(P>0.05).Activities of Na+-K+-ATPase and Ca 2-Mg 2+-ATPase of thoracic aorta smooth muscle cel were negatively relative to blood pressure(r=-0.446、r=-0.387,P<0.01).Conclusion:The changes of calcium transport protein activities of aortic vascular smooth muscle cell play an important role in the development of hypertension.Irbesartan may effectively inhibit the progress of hypertension by elevating calcium transport protein activities of vascular smooth muscel cell.展开更多
文摘目的:探讨阿托伐他汀控制自发性高血压大鼠(SHR)高血压的机制,研究阿托伐他汀对SHR血浆内皮素-1(ET-1)和主动脉一氧化氮合酶(NOS)的影响,以及对SHR的主动脉平滑肌细胞(ASMC)凋亡和P27蛋白表达的影响。方法:选用8周龄SHR 12只,随机分为阿托伐他汀治疗组(ATV组,N=6)和SHR组(N=6),并以同周龄 WKY(N=6)作为对照。ATV组给以阿托伐他汀(50MG·KG-1·D-1)灌胃。10周后观察3组大鼠血压、血清总胆固醇 (TC)、总甘油三酯(TG)含量变化,血浆ET-1和主动脉NOS活性的改变,以及TUNEL法检测ASMC凋亡率,测定动脉 ASMC P27蛋白表达。结果:阿托伐他汀给药10周后,ATV组动脉收缩压显著低于SHR组[(134．17±3．60)MMHG VS (173．33±3．78)MMHG,P<0．01];ATV组血清TC和TG浓度均显著低于SHR组(P<0．01,P<0．01)。同时,阿托伐他汀显著降低SHR血浆ET-1水平[(130．04±40．07)NG/L VS(196．74±59．69)NG/L,P<0．05]和增加SHR主动脉NOS 活性[(0．189±0．040)KU/G PROTEIN VS (0．124±0．057)KU／G PROTEIN,P<0．01];ATV组ASMC凋亡率显著高于SHR组 (16．94％±3．08％ VS 9．01％±2．36％,P<0．01);ATV组ASMC P27蛋白表达阳性率显著高于WKY大鼠(33．02％± 5．01％ VS 24．25％±4．41％,P<0．05),而SHR组该指标明显低于WKY大鼠(16．08％±7．09％ VS 24．25％±4．41％, P<0．05)。结论:阿托伐他汀控制SHR血压增高,其机制可能与降低SHR的血浆ET-1水平和增高主动脉NOS活性,以及增高ASMC凋亡率和P27蛋白表达阳性率有关。
文摘Objective:To investigate the changes of calcium transport protein activities of aortic vascular smooth muscle cell in the progress of hypertension,evaluate the effects of irbesartan on them,then to elucidate the relationship between cell calcium transport protein and hypertension.Methods:Sixteen sixteen-week-old SHR were randomized into irbesartan treated group(IBT group,n=8)and distilled water group(DW group,n=8),and Wistar-Kyoto rats(WKY)as normal controls.Irbesartan and appropriate amounts of distilled water were administered respectively for 14 weeks by gavage.Blood pressure of caudal artery was examined before and after treatment,activities of Na+-K+-ATPase and Ca 2+-Mg 2+-ATPase of thoracic vascular aorta smooth muscle cell were measured.Results:Blood pressure in IBT group was much lower than that in DW group(129.17±3.71)vs(186.50±6.06),P<0.01).Compared with DW group,activities of Na+-K+-ATPase and Ca 2+-Mg 2+-ATPase of thoracic vascular aorta smooth muscle cell were remarkedly higher in both IBT group and WKY group(5.56±0.92)vs(2.91±0.56),P<0.01;(4.83±0.86)vs(2.76±0.43),P<0.01),(5.98±0.63)vs(2.91±0.56),P<0.01;(4.94±0.84)vs(2.76±0.43),P<0.01),while there was a slight difference between IBT group and WKY group(P>0.05).Activities of Na+-K+-ATPase and Ca 2-Mg 2+-ATPase of thoracic aorta smooth muscle cel were negatively relative to blood pressure(r=-0.446、r=-0.387,P<0.01).Conclusion:The changes of calcium transport protein activities of aortic vascular smooth muscle cell play an important role in the development of hypertension.Irbesartan may effectively inhibit the progress of hypertension by elevating calcium transport protein activities of vascular smooth muscel cell.
