α_1肾上腺素能受体介导去甲肾上腺素促大鼠培养心肌细胞蛋白质合成效应

α_1 ADRENERGIC RECEPTOR MEDIATES THE NORADRENALINE INDUCED ENHANCEMENT OG PROTEIN SYNTHESIS IN RAT CULTURED CARDIOMYOCYTE

在无血清和含１．０％、５．０％血清培养的新生大鼠心肌细胞标本上，去甲肾上腺素（ＮＥ，２．０μｍｏｌ／Ｌ）使细胞蛋白质含量（Ｌｏｗｒｙ法）分别比相应对照组增加４０％、２６％、１９％（Ｐ均＜０．０１）；细胞３Ｈ－亮氨酸参入量与ＮＥ浓度呈正性剂量依赖性，最大效应浓度为２０．０μｍｏｌ／Ｌ；无血清培养体系中，０．２、２．０、２０μｍｏｌ／Ｌ的ＮＥ使参入量分别比对照增加１７．８％、３５３％、３７．７％；１．０％血清培养体系中分别比对照增加１６．２％、２７．９％、３１．６％（Ｐ均＜０．０５）；哌唑嗪（２．０μｍｏｌ／Ｌ）可阻断ＮＥ的促蛋白质合成作用，心得安（２．０μｍｏｌ／Ｌ）则无此效应。提示在无血清或低浓度血清培养体系中，ＮＥ可促进心肌细胞蛋白质合成，增加细胞蛋白质含量，该作用可能是通过α１肾上腺素能受体介导。

The effects of α1-adrenergic stimulation on the rate of protein synthesis and the protein con-tent in primary cultures of neonatal rat cardiomyocytes were examined. Treatment ofcardiomyocyte with noradrenaline(NE, 2.0μmol /L) increased total cellular protein content by40%, 26%and 19%(P<0.01) respectively in the serum-free, 1.0% and 5.0% serum-supplementmedia as compared with the control. Addition of NE to the serum-free medium or the mediumwith 1.0% serum-supplement indueed a dose-dependent increase in 3H-leucine incorporationinto cardiomyocyte protein. After addition of0.2,2.0,20.0μmol/L NE, the 3H-leucine incor-poration was increased by 17.8%, 35.3%, 37.7%(P<0 .01) respectively in the serum-free me-dium and by 16.2%, 27.9%,31.6% (P<0.01)in the medium with 10% serum-supplement.Theselective α1-adrenergic antagonists prazosin(2.0μmol/L), but not β-adrenergic blockerpropranolol(2.0μmol/L), effectively inhibited the NE-induced increase in either total cellularprotein or 3H-leucine incorporation. These results suggest that α1-adrenergic stimulation in-creases protein content of cardiomyocytes by accelerating protein synthesis.