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.

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 (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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