冷应激对高血压大鼠交感神经活性及脑干基质交感分子1表达的影响

Effects of cold stress on sympathetic nerve activity and Stim1 expression of rats with hypertension

目的观察冷应激对自发性高血压(SHR)大鼠交感神经活性及脑干基质交感分子1(Stim1)表达的影响。方法选择雄性SHR及正常大鼠各10只,将正常大鼠随机分为正常对照组、单纯冷应激组各5只,SHR大鼠随机分为SHR模型组、SHR冷应激组各5只。正常对照组及模型对照组均置于24℃的代谢笼中6 h,单纯冷应激组及SHR冷应激组均置于4℃代谢笼中6 h进行诱发冷应激。应用Panlab NIBP System无创血压测量系统测量各组大鼠尾动脉收缩压(SBP)、舒张压(DBP);采用代谢笼法收集各组大鼠尿液,高效液相色谱仪检测尿去甲肾上腺素(NE)排泄量。取脑干组织,采用实时定量PCR法检测脑干Stim1 mRNA表达,Western blotting法检测脑干Stim1蛋白表达。结果单纯冷应激组SBP、DBP和尿NE排泄量均高于正常对照组;SHR冷应激组SBP、DBP和尿NE排泄量均高于SHR模型组和单纯冷应激组;SHR冷应激组脑干Stim1 mRNA及蛋白表达均低于SHR模型组和单纯冷应激组(P均<0.01)。结论冷应激下,Stim1可能为调控交感神经活性的关键基因。

Objective To investigate the effects of cold stress on the sympathetic nerve activity and Stim1 expression of spontaneously hypertensive rats（ SHR）. Methods Ten male SHR and 10 normal male rats were selected. The normal male rats were randomly divided into the normal control group and cold stress group,and SHR were randomly divided into the SHR model group and SHR cold stress group,with 5 in each. Rats in the normal control group and SHR model group were placed into metabolic cages at room temperature for 6 h,and the rats in the cold stress group and SHR cold stress group were placed into metabolic cages at 4 ℃ for 6 h. Systolic（ SBP） and diastolic（ DBP） blood pressure was monitored during room temperature and cold stress by tail-cuff method. Urine norepinephrine excretion was detected by HPLC. The mRNA and protein expression of Stim1 in brainstem were detected by quantitative real-time PCR and Western blotting,respectively. Results The SBP,DBP and urinary NE excretion were significantly higher in the cold stress group than in the normal control group; the SBP,DBP,and urinary NE excretion were significantly higher in the SHR cold stress group than in the SHR model group and cold stress group. The Stim1 mRNA and protein expression levels in brainstem were significantly lower in the SHR cold stress group than in the SHR model group and cold stress group（ all P〈0. 01）. Conclusion In response to cold stress,Stim1 may be the key gene to modulate the sympathetic nerve activity.