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机构地区:[1]南京中医学院中医药研究所,南京210029 [2]中国医学科学院药物研究所,北京100050 [3]南京铁道医学院药理教研室,南京210009
出 处:《药学学报》1993年第10期728-731,共4页Acta Pharmaceutica Sinica
摘 要:用Fura-2/AM技术直接观察前胡丙素(Pra-C)对培养大鼠心室肌细胞内游离钙的影响。结果显示Pra-C浓度为0.1~1.0μmol·L^(-1)可明显抑制CaCl_2,高K^+和Bay K 8644引起[Ca^(2+)]i增加,并且有剂量—效应关系,对ouabain引起的[Ca^(2+)]i增加无明显作用。结果提示Pra-C降低心肌细胞[Ca^(2+)]i的作用与抑制电压依赖性钙通道有关。The negative inotropic effect of Pra-C was supposed to be related to the blocking of extracellular calcium influx but direct evidence is not known. We, therefore, examined the effects of PraC on [Ca^(2+)] i in isolated rat ventricular myocytes using the fluorescent Ca^(2+)- indicator Fura-2/AM. It was found that Pra-C inhibited the elevation of [Ca^(2+)]i induced by potassiumdepolarization, high extracellular calcium and calcium agonist Bay K 8644 in a dose-dependent manner. At 1.0 μmol · L^(-1), it decreased the [Ca^(2+)]i at the presence of 75 mmol · L^(-1) KCl, 10 mol · L~^(-1) CaCl and 3 μmol · L^(-1) Bay K 8644 by 50, 31 and 42% respectively. No significant effect on ouabain evoked [Ca^(2+)]i increase was found, showing that it does not affect sarcolemmal Na^+ —Ca^(2+)exchange. These results further indicate that Pra-C may decrease the [Ca^(2+)]i of myocyte by blocking voltage-dependent calcium channels.
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