【摘要】：目的觀察冷應激對自發(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,將正常大鼠隨機分為正常對照組、單純冷應激組各5只,SHR大鼠隨機分為SHR模型組、SHR冷應激組各5只。正常對照組及模型對照組均置于24℃的代謝籠中6 h,單純冷應激組及SHR冷應激組均置于4℃代謝籠中6 h進行誘發(fā)冷應激。應用Panlab NIBP System無創(chuàng)血壓測量系統(tǒng)測量各組大鼠尾動脈收縮壓(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尿去甲腎上腺素(NE)排泄量。取腦干組織,采用實時定量PCR法檢測腦干Stim1 mRNA表達,Western blotting法檢測腦干Stim1蛋白表達。結(jié)果單純冷應激組SBP、DBP和尿NE排泄量均高于正常對照組;SHR冷應激組SBP、DBP和尿NE排泄量均高于SHR模型組和單純冷應激組;SHR冷應激組腦干Stim1 mRNA及蛋白表達均低于SHR模型組和單純冷應激組(P均0.01)。結(jié)論冷應激下,Stim1可能為調(diào)控交感神經(jīng)活性的關鍵基因。
[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：2297706