Sparrow M P, Mitchell H W, Everett A W
Department of Physiology, University of Western Australia, Sydney.
Basic Res Cardiol. 1990 Mar-Apr;85(2):209-16. doi: 10.1007/BF01906973.
The relative proportion of the two putative heavy chains of smooth muscle myosin (MHC1 and MHC2) was determined in the caudal and femoral arteries of spontaneously hypertensive rats (SHR) and normotensive (WKY) rats at 16 weeks of age. The heavy chain polypeptides with Mr 204,000 and 200,000 were resolved electrophoretically under denaturing conditions in porous polyacrylamide gels. Both proteins reacted strongly with a monoclonal antibody (2C4) to smooth muscle MHC. In caudal arteries the ratio of MHC1/MHC2 was 3.1:1 in SHR rats compared with 1.8:1 in WKY rats (p less than 0.005) and similarly in femoral arteries, 2.8:1 vs 1.5:1 (p less than 0.001). In the portal vein there was no significant difference, 1.7:1 vs 1.5:1. The possibility that the higher MHC ratio in the SHR is the genetically mediated defect in arterial smooth muscle cells leading to the hypertension is discussed as an alternative to the elevated systemic blood pressure causing the altered MHC ratio.
在16周龄的自发性高血压大鼠(SHR)和正常血压(WKY)大鼠的尾动脉和股动脉中,测定了平滑肌肌球蛋白两条假定重链(MHC1和MHC2)的相对比例。在变性条件下,通过多孔聚丙烯酰胺凝胶电泳分离出分子量为204,000和200,000的重链多肽。这两种蛋白质都能与平滑肌MHC的单克隆抗体(2C4)发生强烈反应。在尾动脉中,SHR大鼠的MHC1/MHC2比值为3.1:1,而WKY大鼠为1.8:1(p<0.005);在股动脉中情况类似,分别为2.8:1和1.5:1(p<0.001)。在门静脉中,两者无显著差异,分别为1.7:1和1.5:1。讨论了SHR中较高的MHC比值是导致高血压的动脉平滑肌细胞遗传介导缺陷这一可能性,作为对升高的全身血压导致MHC比值改变的另一种解释。