Pyk2在Goldblatt鼠左心室肥大心肌中的变化

The changes of Pyk2 mediated signal transduction in the myocardium of Goldblatt rats

目的以两肾一夹肾性高血压大鼠为模型,研究肥大心肌中富脯氨酸蛋白酪氨酸激酶(Pyk2)介导的细胞信号转导的变化及其意义。方法制备两肾一夹肾性高血压大鼠模型,分别于术后第1、4、8和12周测定尾动脉血压和心肌肥大指数,免疫组织化学法检测肥大心肌组织中Pyk2及其磷酸化表达。结果大鼠肾动脉狭窄术后4周心肌肥大已发生,8周至12周心肌肥大进一步加重;术后4、8、12周大鼠心肌组织Pyk2活性逐渐增加,心肌Pyk2活性与心肌肥大程度呈显著正相关。结论随肾动脉狭窄时间的延长,Pyk2活性逐渐增加是导致心肌肥大加剧的重要原因;Pyk2非受体酪氨酸激酶介导的信号通路可能是心肌肥大的重要的信号通路。

Objective To investigate the changes of Pyk2 （ proline - rich tyrosine kinase 2） mediated signal transduction in the myocardium of renovascular hypertensive rats（ RHR of Goldblatt）. Methods Two - kidney and one - clip （2K1C） RHR model was established in Spraque- Dawley rats by chronic partial occlusion of the left renal artery. The ratio of left ventricular mass to body weight （LVW/BW） was calculated to indicate the degree of myocardial hypertrophy. Pyk2 protein expression and phosphorylation were determined by immunohistochemisry. Results Blood pressure, LVW/ BW ratio and Pyk2 activity, all increased gradually in the myocardium of RHRs. There was a significantly positive correlation between Pyk2 activity and myocardial hypertrophy. Conclusion Along with the persistence of renal artery stenosis, the increase of Pyk2 activity must be an important factor causing the advance of cardiac hypertrophy, as Pyk2 signaling is a novel Ca2 ＋ - dependent pathway leading to cardiac hypertrophy.