Substance P is associated with hypothalamic paraventricular nucleus activation that coincides with increased urotensin 2 mRNA in chicks

Exogenous administration of substance P (SP) exerts anorexigenic effects in both chicks and rats, but the central mechanism mediating this response is poorly understood. Therefore, this study was designed to elucidate mechanisms of SP-induced anorexia using chicks as models. Chicks that received intracerebroventricular (ICV) injections of SP dose-dependably reduced their food intake with no effect on water intake. Next, the diencephalon was isolated from SP-injected chicks and mRNA expression of neuropeptide Y (NPY), corticotropin releasing factor (CRF), urocortin 3 (UCN 3) and CRF receptors were measured but were not affected. When measured in the hypothalamus, mRNA abundance of these and NPY receptors, urotensin 2 (UTS2) and melanocortin receptor 4 (MCR4) were not affected by SP-injection. Quantification of c-Fos immunoreactivity in appetite-associated hypothalamic nuclei demonstrated that the paraventricular nucleus (PVN) was activated in SP-injected chicks. Finally, in the PVN isolated from SP-injected chicks, there was increased expression of UTS2 mRNA while CRF and UCN3 were not affected. Thus, the anorexigenic effects of SP appear to be mediated by PVN activation and may involve UTS2.     

肺动脉高压相关因子的研究进展

肺动脉高压是不同病因导致的、以肺动脉压力和肺血管阻力升高为特点的一组病理生理综合征.其复杂的发病机制仍未完全明了,但近年来随着人们对肺动脉高压发病机制认识的不断深入,发现一些使肺血管舒缩及重塑的因子在肺动脉高压形成过程中发挥着极其重要的作用.本文主要阐述低氧诱导因子1、尾加压素Ⅱ、降钙素基因相关肽、血管生成素1在肺动脉高压中的作用机制.     

尾加压素Ⅱ及其受体系统在糖尿病大鼠心血管及肾脏组织中的表达

目的观察糖尿病大鼠心肌、主动脉、肾脏组织中尾加压素Ⅱ（urotensinⅡ,UⅡ）、尾加压素Ⅱ相关肽（urotensinⅡ—related peptide,URP）及其G蛋白耦联受体14（G-protein—coupled receptor 14,GPR14）表达的变化,以探讨UⅡ-URP—GPR14系统在糖尿病相关并发症中的作用。方法30只Wistar雄性大鼠,分为对照组及糖尿病组,糖尿病组由链脲佐菌素（streptozotocin,STZ）诱导成模,喂养5个月后,实时PCR法测定心肌、主动脉、肾脏组织UⅡ、URP及GPR14的表达。结果糖尿病大鼠各心腔及肾脏组织的UⅡ基因表达明显增加,URP基因表达仅在主动脉和肾脏组织增加,它们的共同受体GPR14基因表达在各心腔及主动脉、肾脏组织均明显增加。结论UⅡ—URP—GPR14系统可能参与糖尿病性心、肾、血管并发症的发病。     

Role of urotensin II and its receptor in health and disease

Urotensin II (U-II) is currently the most potent vasoconstrictor identified. This action is brought about via activation of a G_q/11-protein coupled receptor (UT receptor). U-II activation of the UT receptor increases inositol phosphate turnover and intracellular Ca²⁺. In addition to producing vasoconstriction, dilation and ionotropic effects have also been described. There is considerable variation in the responsiveness of particular vascular beds from the same and different species, including humans. Receptors for U-II are located peripherally on vascular smooth muscle (contractile responses) and endothelial cells (dilatory responses via nitric oxide). In humans, plasma U-II is elevated in heart failure, renal failure, liver disease, and diabetes. Iontophoresis of U-II in healthy volunteers produces vasodilation (of the forearm) while in patients with heart failure or hypertension a constriction is observed. To date there is only one clinical study using a UT receptor antagonist (palosuran) in diabetic patients with macroalbuminuria. This antagonist reduced albumin excretion, probably by increasing renal blood flow. Studies in other disease conditions are eagerly awaited. In summary, the U-II / UT receptor system has clinical potential, and for the anesthesiologist, this novel peptide-receptor system may be of use in the intensive care unit.     

早期糖尿病大鼠肾组织尾加压素Ⅱ表达的实验研究

目的：探讨早期糖尿病大鼠肾组织中尾加压素Ⅱ（urotensin Ⅱ,UⅡ）的表达及其意义。方法：用链脲佐菌素（STZ）诱导糖尿病大鼠模型,将实验动物分为正常对照组（C组）、糖尿病组（D组）和胰岛素干预组（Y组）。5周后收集肾组织,观察各组肾脏病理情况及UⅡ在肾组织中的表达。结果：处理5周后,与C、Y组比较,D组肾小球肥大、肾小球表面积显著增大,小管扩张,上皮细胞肿胀;D组肾小管上皮细胞UⅡ表达明显升高（与C组比较,P〈0.05）;Y组肾小管上皮细胞UⅡ表达有不同程度的下降（与D组比较,P〈0.05）。结论：STZ诱导的早期糖尿病大鼠肾小管上皮细胞UⅡ表达明显上调;应用胰岛素严格控制血糖可部分下调肾组织UⅡ的表达。UⅡ在STZ诱导的早期糖尿病大鼠肾脏病变的发展过程中可能起一定作用。     

尾加压索Ⅱ与糖尿病视网膜病变的相关性研究

目的:探讨尾加压索Ⅱ与糖尿病视网膜病变的关系.方法:采用放射免疫分析法检测糖尿病视网膜病变患者(DR)90例和正常对照组(D组)30例血浆中尾加压索Ⅱ的水平,DR患者行直接眼底镜和眼底荧光血管造影检查,按分期定为A、B、C组,检测并比较4组糖化血红蛋白(HbA1c)和尿白蛋白排泄率(UAER),并分析相互的相关性.结果:糖尿病视网膜病变各组患者血浆中尾加压索Ⅱ水平较正常对照组显著升高(P均＜0.01),与HbA1c、UAER呈显著正相关(P＜0.01).结论:血清尾加压索Ⅱ与2型糖尿病视网膜病变密切相关,其浓度的测定对判断2型糖尿病视网膜病变的发生、发展有重要的临床意义.     

尾加压素Ⅱ对培养乳鼠心肌细胞内钙离子的影响及其机制

目的 观察尾加压素Ⅱ（UⅡ）对体外培养乳鼠心肌细胞内钙离子浓度的影响。方法把体外培养的SD乳鼠心肌细胞以Fluo3／AM荧光指示剂负载,分为4组：正常对照组;单纯UⅡ干预组;尼卡地平提前阻断＋UⅡ干预组;IP3受体拮抗剂XestsponginC＋UⅡ干预组。应用激光共聚焦显微镜技术检测心肌细胞钙离子浓度变化。结果正常对照组心肌细胞内钙离子荧光强度较低（31．65±2．37）;单纯UⅡ干预组钙离子荧光强度增加明显（87．13±5．72）;尼卡地平提前阻断＋UⅡ干预组以及IP3受体拮抗剂XestsponginC＋UⅡ干预组钙离子也有增加,分别为（59．43±4．76）、（54．79±5．18）。结论UⅡ可引起心肌细胞内钙离子浓度增高,其主要的机制可能与细胞外钙离子内流和肌浆网钙离子释放增加有关。     

联合降压治疗对高血压病患者外周血中血管活性物质的影响及意义

目的观察非洛地平联合坎地沙坦对高血压患者血浆尾加压素Ⅱ（UⅡ）、脂联素（ADI）和血管紧张素Ⅱ（Ang Ⅱ）的影响。方法将88例入选患者作为治疗组,24例健康人群作为对照组,治疗组给予非洛地平及坎地沙坦治疗,测定治疗组患者药物治疗前后的外周血和对照组外周血中UⅡ、ADI、AngⅡ变化。结果治疗组UⅡ和AngⅡ水平高于对照组（t=3.961和t=2.816,均P〈0.01）,ADI低于对照组（t=16.243,P〈0.01）。治疗组治疗后较治疗前血压下降明显（P〈0.01）;UⅡ降低（t=2.024,P〈0.05）,ADI升高（t=5.589,P〈0.01）。结论非洛地平联合坎地沙坦可降低高血压患者外周血UⅡ水平,升高ADI、Ang Ⅱ水平。降低血压后,减轻了对ADI的抑制,减少了对UⅡ释放的诱导,提示联合降压治疗对高血压患者具有血管保护作用。     

全麻对手术病人血浆尾加压素Ⅱ和肾素、血管紧张素活性的影响

目的：研究全麻诱导地患者血浆加压素Ⅱ和肾素、血管紧张素活性的影响。方法：20例全麻手术患者,于麻醉诱导前20分钟和诱导后10分钟分别抽取静脉血测定血浆尾加压素Ⅱ和肾素、血管紧张素活性。结果：与麻醉前比较,麻醉后尾加压素Ⅱ的浓度明显下降（P＜0．01）;肾素活性及血管加压素Ⅱ含量均明显升高（P＜0．01）。结论：全麻后,血浆尾加压素Ⅱ与肾素、血管紧张素含量呈反向变化。     

妊娠高血压综合征孕妇血浆尾加压素Ⅱ与血清C反应蛋白检测水平的临床意义

目的 探讨妊娠高血压综合征(pregnancy-induced hypertension syndrome,PIH)孕妇血浆尾加压素Ⅱ(urotensin Ⅱ,UII)与血清C反应蛋白(C-reactive protein,CRP) 检测水平的临床意义.方法 采用酶联免疫吸附法(enzyme-linked immuno...