The behavioural effects of corticotropin-releasing factor-related peptides in rats

The present study determined the behavioural effects of the corticotropin releasing factor (CRF)-related peptides, human/rat CRF (h/rCRF), ovine CRF (oCRF), sauvagine (SAUV), urotensin I (UT) and the recently discovered neuropeptide, rat urocortin (rUCN). All of the peptides dose-dependently increased motor activity in a familiar environment and reduced feeding in hungry rats. There was no apparent relationship between potency/affinity at CRF₂ receptors and effects in these two tests. In a comparison of h/rCRF and rUCN upon discrete spontaneous behaviours, both peptides (3.0 μg ICV) increased activity and grooming, induced a fore-paw tremor and reduced the incidence of motionlessness. However, h/rCRF reduced motionlessness to a greater extent and was a more potent inducer of defaecation, weight loss, oral movements and fore-paw tremor than rUCN. In the elevated X maze, both h/rCRF and rUCN (1.0 μg ICV) had anxiogenic-like effects upon behaviour. In contrast, h/rCRF (1.0 μg ICV), but not rUCN (1.0–10 μg ICV) increased the startle response to an acoustic stimulus. In summary, all the CRF-related peptides increased motor activity and reduced feeding in rats in a similar manner and both rUCN and h/rCRF induced anxiogenesis. However, there were some behavioural differences between rUCN and h/rCRF which require further study. Further pharmacological investigation of the role of CRF receptor subtypes requires the use of subtype selective antagonists. Received: 8 January 1997/Final version: 24 January 1998     

Does cigarette smoking increase plasma urotensin II concentrations?

Objective Human urotensin II (UII) acts on the urotensin (UT) receptor and is the most potent mammalian vasoconstrictor identified to date. The role of UII in human cardiovascular regulation remains unclear, and the results of plasma measurements have been conflicting, perhaps because different measurement techniques have been used. The effects of cigarette smoking on plasma UII concentrations are unknown. The primary aim of our study was to demonstrate whether cigarette smoking had any effect on plasma UII concentrations in otherwise healthy volunteers. Our secondary aim was to compare the results obtained from assaying simultaneously using both radioimmunoassay (RIA) and immunoluminometric assay (ILMA). Methods Blood was taken from 20 healthy male non-smokers and 20 healthy male cigarette smokers. Plasma was separated and stored at −70°C. Samples were batch analysed simultaneously for UII using RIA and ILMA. Results Median (range) plasma UII concentrations were lower in non-smokers [1.67 (1.0–2.27) pg ml⁻¹] compared to smokers [2.62 (1.87–3.46) pg ml⁻¹] (P = 0.03) measured using RIA. Those who had smoked a cigarette in the 10 min before sampling had greater concentrations of UII [3.10 (1.87–4.60) pg ml⁻¹] compared to controls (P = 0.01). Plasma UII concentrations determined by ILMA were consistently low with no differences between groups. Conclusion The data obtained by RIA show that smoking may increase plasma concentrations of UII with a more pronounced increase when a cigarette has been smoked recently. There was a complete lack of correlation between RIA and ILMA for the whole data set, which suggests that some of the variability in plasma UII reported in the literature may result from differences between assays. Presented in part at the Anaesthetic Research Society meeting, Leicester, UK, 24 November 2005.     

老年高血压患者踝肱指数与尾加压素Ⅱ相关性研究

目的：研究老年高血压患者踝肱指数与尾加压素Ⅱ（UⅡ）的相关性,进一步探讨UII与动脉粥样硬化的关系。方法：采用放免法测定130例老年高血压患者及72例健康老年人血浆UⅡ浓度,并分别测量踝肱指数（anklebrachialindex,ABI）,再根据ABI严重程度将高血压患者分为ABIO、ABI1、ABI2三组。结合UⅡ水平、踝肱指数对各组进行比较分析。结果：与健康组比较,高血压患者踝肱指数明显降低,而血浆UⅡ水平明显升高（P〈0．01）;高血压患者血浆UⅡ水平与ABI呈明显负相关,高血压三组UⅡ水平组间比较差异有统计学意义（P〈0．05）。结论：老年高血压患者的踝肱指数与血浆uⅡ水平呈负相关,提示UⅡ浓度与动脉粥样硬化密切相关。     

尾加压素Ⅱ及其与肿瘤的关系

尾加压素Ⅱ(U-Ⅱ)是一种新发现的血管活性肽,通过激活G蛋白耦联受体,引起胞外钙内流、胞内钙贮释放而发挥作用.经研究证实U-Ⅱ在多种肿瘤细胞中均有表达,其在肿瘤生长、转移过程中所发挥的作用值得进一步研究.     

尾加压素Ⅱ与代谢综合征

目的：探讨尾加压素Ⅱ与代谢综合征的关系。方法：查阅相关中外文献,分析尾加压素Ⅱ与代谢综合征的关系。结果：尾加压素Ⅱ与高血糖、高血压、胰岛素抵抗等代谢综合征大部分组成成分相关。结论：通过对尾加压素Ⅱ的研究,进一步提高对代谢综合征的认识。     

检测子痫前期患者尾加压素Ⅱ及内皮型一氧化氮合酶的临床意义研究

目的探讨检测子痫前期孕妇血中尾加压素Ⅱ（UⅡ）与内皮型一氧化氮合酶（eNOS）含量的临床意义。方法选择我院产科收治的子痫前期孕妇30例（实验组）及普通孕妇30例（对照组）,采用ELISA法分别检测2组孕妇血中的尾加压素Ⅱ及内皮型一氧化氮合酶的含量水平值,并对检测结果进行对比分析。结果实验组尾加压素Ⅱ含量水平值（3．27±1．12）μmol／L明显高于对照组孕妇（1．91±0．39）μmol／L;对照组内皮型一氧化氮合酶含量水平值（89．33±25．79）μmol／L明显低于实验组（125．67±34．36）μmol／L,差异均有统计学意义（P〈0．05）。结论通过检测孕妇血中eNOS与UⅡ水平可反映该病的发展情况,可作为该病的辅助指标,为临床早期监控及治疗提供重要的价值。     

Urantide对动脉粥样硬化大鼠脾组织中ERK1/2及P38表达的影响

目的 观察Urantide对动脉粥样硬化（atherosclerosis,AS）大鼠脾组织中MAPK信号通路ERK1/2和P38蛋白表达的影响,探究Urantide抗AS大鼠脾损伤的作用及机制。 方法 180只Wistar大鼠随机分为：正常组,模型组,辛伐他汀组,Urantide 3 d、7 d、14 d组。HE染色观察大鼠胸主动脉、脾组织;免疫组织荧光染色、Western blot检测大鼠脾中ERK1/2、P38蛋白表达。 结果 AS组与正常组相比,大鼠胸主动脉内出现典型AS病变,脾中央动脉出现玻璃样变,大鼠脾中p-ERK1/2、p-P38蛋白阳性表达升高（P<0.05）。Urantide各组与AS组相比,脾组织中玻璃样病变减轻,脾内p-ERK1/2、p-P38蛋白阳性表达降低,其中以Urantide 14 d组最明显（P<0.05）。 结论 Urantide可通过抑制ERK1/2、P38的表达,发挥抗AS作用,进而改善AS大鼠脾组织病变程度。     

糖尿病大鼠血浆尾加压素Ⅱ的变化及厄贝沙坦干预的影响

目的探讨尾加压素Ⅱ（UⅡ）水平在糖尿病大鼠血浆中的变化及厄贝沙坦对其影响。方法选择30只Wistar雄性大鼠为对照组。链脲佐菌素（STZ）诱导的糖尿病大鼠54只随机分为糖尿病未干预组及糖尿病干预组各27只。糖尿病于预组给予厄贝沙坦灌胃,其余2组给予相同体积的蒸馏水灌胃,给药4周,给药前后测定血糖及血浆UⅡ水平。结果用药前后各组大鼠血糖变化差异无统计学意义（P〉0．05）;糖尿病大鼠UⅡ明显高于对照组（P〈0．01）;糖尿病干预组用药后UⅡ降低（P〈0．05）,且低于糖尿病未干预组（P〈0．05）。结论UⅡ系统活化可能在糖尿病的病程中发挥重要作用并可能受到RAS系统的调控。     

黄芪对尾加压素Ⅱ诱导的心脏成纤维细胞胶原合成及分泌转化生长因子-β_1的影响

目的观察黄芪注射液对尾加压素Ⅱ（UⅡ）诱导的心脏成纤维细胞合成胶原及分泌转化生长因子（TGF-β1）的影响。方法体外培养乳鼠心脏成纤维细胞,分成3组：对照组、UⅡ组、UⅡ＋黄芪组。作用一定时间后,Real-time RT-PCR法测定各组细胞Ⅰ、Ⅲ型胶原及TGF-β1基因表达情况,3H-脯氨酸掺入测定胶原合成情况,双抗体夹心ELISA法测定培养上清TGF-β1分泌情况。结果UⅡ可以促进乳鼠心脏成纤维细胞胶原合成,刺激TGF-β1的分泌,黄芪注射液可明显抑制UⅡ的上述作用。结论黄芪可以通过抑制UⅡ诱导的心脏成纤维细胞胶原合成及TGF-β1分泌,延缓心肌纤维化及心脏重构的进展。