【摘要】：目的觀察冷應(yīng)激對(duì)自發(fā)性高血壓(SHR)大鼠交感神經(jīng)活性及腦干基質(zhì)交感分子1(Stim1)表達(dá)的影響。方法選擇雄性SHR及正常大鼠各10只,將正常大鼠隨機(jī)分為正常對(duì)照組、單純冷應(yīng)激組各5只,SHR大鼠隨機(jī)分為SHR模型組、SHR冷應(yīng)激組各5只。正常對(duì)照組及模型對(duì)照組均置于24℃的代謝籠中6 h,單純冷應(yīng)激組及SHR冷應(yīng)激組均置于4℃代謝籠中6 h進(jìn)行誘發(fā)冷應(yīng)激。應(yīng)用Panlab NIBP System無創(chuàng)血壓測(cè)量系統(tǒng)測(cè)量各組大鼠尾動(dòng)脈收縮壓(SBP)、舒張壓(DBP);采用代謝籠法收集各組大鼠尿液,高效液相色譜儀檢測(cè)尿去甲腎上腺素(NE)排泄量。取腦干組織,采用實(shí)時(shí)定量PCR法檢測(cè)腦干Stim1 mRNA表達(dá),Western blotting法檢測(cè)腦干Stim1蛋白表達(dá)。結(jié)果單純冷應(yīng)激組SBP、DBP和尿NE排泄量均高于正常對(duì)照組;SHR冷應(yīng)激組SBP、DBP和尿NE排泄量均高于SHR模型組和單純冷應(yīng)激組;SHR冷應(yīng)激組腦干Stim1 mRNA及蛋白表達(dá)均低于SHR模型組和單純冷應(yīng)激組(P均0.01)。結(jié)論冷應(yīng)激下,Stim1可能為調(diào)控交感神經(jīng)活性的關(guān)鍵基因。
[Abstract]:Objective to observe the effects of cold stress on sympathetic nerve activity and brain stem matrix sympathetic molecule 1 (Stim1) expression in spontaneously hypertensive (SHR) rats. Methods 10 male SHR rats and 10 normal rats were randomly divided into normal control group (n = 5), cold stress group (n = 5), SHR model group (n = 5) and SHR cold stress group (n = 5). The normal control group and the model control group were placed in the metabolic cage at 24 鈩，

本文編號(hào)：2297706