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（２０ｍｇ·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±３６ｆｍｏｌ·ｍｇ￣（－１）ｖｓ８３６±４７ｆｍｏｌ·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。
m-Nifedipine(m-Nif 20 mg·kg-1·d-1 ig)was administered orally to male deoxvcorti-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 ptessure,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 blcod pressure.
出处
《药学学报》
CAS
CSCD
北大核心
1996年第5期333-339,共7页
Acta Pharmaceutica Sinica
基金
国家自然科学基金
关键词
间硝苯地平
心肌肥厚
结合位点
二氢吡啶
m-Nifedipine
Cardiac mass
Binding sites
Dihydropytidine
Deoxycorticosterone acetate
