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 deoxycorticosterone-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 hypertrophied LV. The density (Bmax) and the total number of DHP binding sites in hypertrophied 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.
Xu
Y
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Laboratory of Cardiovascular Pharmacology, Nanjing Medical University.
Rao
M R
MR
D000818:Animals; D001665:Binding Sites / Q000187:drug effects; D002118:Calcium / Q000378:metabolism; D002121:Calcium Channel Blockers / Q000494:pharmacology*; D003900:Desoxycorticosterone; D004095:Dihydropyridines / Q000378:metabolism*; D006973:Hypertension / Q000139:chemically induced / Q000378:metabolism*; D017379:Hypertrophy, Left Ventricular / Q000139:chemically induced / Q000378:metabolism*; D008297:Male; D008929:Mitochondria, Heart / Q000378:metabolism; D009543:Nifedipine / Q000494:pharmacology*; D051381:Rats; D017207:Rats, Sprague-Dawley
D002121:Calcium Channel Blockers; D004095:Dihydropyridines; D003900:Desoxycorticosterone; D009543:Nifedipine; D002118:Calcium