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从整体和细胞水平观察血管紧张素Ⅱ(AngⅡ)对心肌细胞血小板源生长因子(PDGF)受体-β表达的影响, 探讨其可能的胞内信号转导机制. 制备2K1C肾性高血压大鼠模型, 术后4和8周测定尾动脉收缩压、心肌肥厚指数和心脏AngⅡ含量; 采用免疫印迹法测定心脏PDGF受体-β含量. 培养乳鼠心 肌细胞, 观察AngⅡ刺激后PDGF受体-β的变化及药物对AngⅡ引起PDGF受体-β改变的影响. 2K1C大鼠术后4, 8周心脏AngⅡ含量增加, PDGF受体-β的含量分别升高了100.3%和127.1%. 这一反应可被captopril所抑制. 在培养的心肌细胞, AngⅡ刺激PDGF受体-β含量增加47.1%, AT1受体拮抗剂losartan可完全抑制AngⅡ所致PDGF受体-β上调. 磷脂酶C(PLC)抑制剂U73122和细胞外信号调节激酶(ERK)上游激酶的抑制剂PD98059可部分抑制AngⅡ上调PDGF受体-β的作用. 因此, AngⅡ可通过其膜受体AT1介导心肌细胞PDGF受体-β上调, 这一作用至少部分地是PLC和ERK依赖的.
To investigate the effect of Ang Ⅱ on the expression of platelet-derived growth factor (PDGF) receptor-β in cardiomyocytes and to explore its possible mechanism of intracellular signal transduction.Methods 2K1C renal hypertensive rats The systolic blood pressure, cardiac hypertrophy index and cardiac Ang Ⅱ content were measured at 4 and 8 weeks after operation, and the content of PDGF receptor-β was measured by Western blotting.Peripheral blood mononuclear cells And the effects of drugs on Ang II-induced changes of PDGF receptor-β.At 4 weeks and 8 weeks after operation, AngⅡcontent increased and the content of PDGF receptor-β increased by 100.3% and 127.1%, respectively Can be inhibited by captopril.In the cultured cardiomyocytes, AngⅡstimulated the increase of PDGF receptor-β content by 47.1% and the AT1 receptor antagonist losartan completely inhibited AngⅡ-induced PDGF receptor-β upregulation. PD98059, an inhibitor of U73122 and an upstream kinase of extracellular signal-regulated kinase (ERK), partially inhibits the up-regulation of PDGF receptor-β by AngⅡ. Therefore, AngⅡ mediates the upregulation of PDGF receptor-β in cardiomyocytes via its membrane receptor AT1 , At least part of this role Sub-ground is PLC and ERK dependent.