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

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。

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

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 (B_max) 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 (K_D) 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.