徐毅, 饶曼人. 间硝苯地平对DOCA-satl 高血压大鼠心肌膜碎片二氢吡啶结合位点的影响J. 药学学报, 1996, 31(1): 333-339.
引用本文: 徐毅, 饶曼人. 间硝苯地平对DOCA-satl 高血压大鼠心肌膜碎片二氢吡啶结合位点的影响J. 药学学报, 1996, 31(1): 333-339.
Y Xu, MR Rao. EFFECTS OF M-NIFEDIPINE ON DIHYDROPYRIDINE BINDING SITES IN HYPERTROPHIED LEFT VENTRICULAR CELL MEMBRANES FROM DEOXYCORTICOSTERONE ACETATE-SALT HYPERTENSIVE RATSJ. Acta Pharmaceutica Sinica, 1996, 31(1): 333-339.
Citation: Y Xu, MR Rao. EFFECTS OF M-NIFEDIPINE ON DIHYDROPYRIDINE BINDING SITES IN HYPERTROPHIED LEFT VENTRICULAR CELL MEMBRANES FROM DEOXYCORTICOSTERONE ACETATE-SALT HYPERTENSIVE RATSJ. Acta Pharmaceutica Sinica, 1996, 31(1): 333-339.

间硝苯地平对DOCA-satl 高血压大鼠心肌膜碎片二氢吡啶结合位点的影响

EFFECTS OF M-NIFEDIPINE ON DIHYDROPYRIDINE BINDING SITES IN HYPERTROPHIED LEFT VENTRICULAR CELL MEMBRANES FROM DEOXYCORTICOSTERONE ACETATE-SALT HYPERTENSIVE RATS

  • 摘要: 用 DOCA-salt 高血压大鼠心肌肥厚模型,观察间硝苯地平(m-Nif)对肥厚心肌膜碎片二氢吡啶(DHP)结合位点的影响。结果显示:预防或治疗性给予m-Nif(20 mg·kg-1·d-1)12 或 9 周,血压降低,心室重和心肌线粒体钙含量减少,且肥厚心肌DHP结合位点密度显著降低(450±25, 462±36 fmol·mg-1 vs 836±47 fmol·mg-1 protein, P<0.001)。提示:m-Nif预防和逆转DOCA-salt 高血压大鼠心肌肥厚的作用可能与其减少肥厚心肌DHP 结合位点密度和血压降低有关。

     

    Abstract: m-Nifedipine(m-Nif 20 mg·kg-1·d-1 ig) was administered orally to male deoxycorti-costerone-acetate-salt(DOCA) hypertensive rats for 9 or 12 wk, the affinity and density of dihydropyridines (DHP) binding sites in the membranes of left ventricle (LV) were investigated. Treatment with m-Nif, whether for prevention (6 wk postoperation) or regression (9 wk postoperation) lowered systolic blood pressure, decreased the weight of left ventricle and the Ca2+ concentration in mitochondria in gypertrophied LV. The density (Bmax) and the total number of DHP binding sites in gypertrophied LV were also markedly decreased (450±25, 462±36 fmol·mg-1 vs 836±47 fmol·mg-1 protein, P<0.001). There was no difference between groups in constant (KD) values of DHP binding sites. These results indicate that m-Nif prevented and regressed cardiac mass in DOCA hypertensive rats through mechanisms that may be associated with their density of DHP binding sites and control of blood pressure.

     

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