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find Keyword "血管紧张素Ⅱ" 15 results
  • CHANGES OF SPLANCHNIC VASCULAR ANGIOTENSIN Ⅱ RECEPTORS IN RATS WITH PORTAL HYPERTENSION

    To investigate the mechanisms of splanchnic hyperdynamics in portal hypertension (PHT), angiotensin Ⅱ(A-Ⅱ) receptor maximal binding capacity (Bmax) and dissociation constants (Kd) of splanchnic blood vessels in rats with prehepatic PHT were studied by radioligand binding analysis. The results showed that the A-Ⅱ receptor Bmax in the superior mesenteric artery and portal vein of PHT animals (206.9±39.3 fmol/mg protein and 31.5±9.2 fmol/mg protein respectively) was all significantly lower than that of the controls (297.2±44.7 fmol/mg protein and 53.4±12.1 fmol/mg protein respectively, P<0.01). The A-Ⅱ receptor Kd in the superior mesenteric artery was markedly increased in PHT animals (1.03±0.11 nmol/L) compared with that in controls (0.88±0.08 nmol/L, P<0.05). In the portal vein, the A-Ⅱ receptor Kd in PHT animals was slightly higher than in controls, but no significant difference was observed between the two groups. These results suggest that the vascular hyporesponsiveness to A-Ⅱ in PHT is caused partially by a reduction in number and a decrease in affinity of vascular A-Ⅱ receptors, and these changes may possibly lead to the formation of hyperdynamic circulation.

    Release date:2016-08-29 03:19 Export PDF Favorites Scan
  • Simvastatin can prevent hypoxic pulmonary hypertension in rats through suppressing the expression of Angiotensin Ⅱ Receptor-1

    Objective To investigate the preventive effect of simvastatin,a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor,on hypoxic pulmonary hypertension and the relation between it and the angiotensin Ⅱ receptor-1(AT1R) expression in pulmonary arteriole.Methods Thirty male Sprague-Drawley rats were randomly allocated into three groups:a control group,a hypoxic group and a simvastatin preventive group.The animal model of hypoxic pulmonary hypertension was established by exposing the rats to normobaric hypoxic condition(8 h×6 d×3 w),and the preventive group were treated with simvastatin 10 mg/kg before hypoxic processing while the control and hypoxic groups were treated with sodium chloride.The mean pulmonary pressure(mPAP),serum cholesterol concentration,right ventricular hypertrophy index [RV/(LV+S)],percentage of the wall thickness in the external diameter(WT%),percentage of the wall area in the total vascular area(WA%),and the AT1R expression in pulmonary arterioles were measured.Results When compared with the hypoxic group,in the preventive group,the mPAP and RV/(LV+S)obviously reduced [(22.6±3.86)mm Hg vs (29.3±2.27)mm Hg,(25.13±0.75)% vs (33.18±1.58)%,Plt;0.01 respectively],the indices of wall thickness of rat pulmonary arteriole and area also decreased significantly [WT%:(15.98±1.96)% vs (25.14±1.85)%;WA%:(54.60±3.94)% vs 74.77±4.52)%;Plt;0.01 respectively],and the positive degree of AT1R still lessened noticeably(1.23±0.09 vs 1.57±0.13,Plt;0.01).All of the indices above in the hypoxic group increased markedly compared with the control group(Plt;0.01 respectively).However,the differences of serum cholesterol among three groups were not significant(Pgt;0.05).Conclusions Simvastatin can suppress the expression of AT1R in pulmonary vessel and prevent hypoxic pulmonary hypertension.

    Release date:2016-08-30 11:35 Export PDF Favorites Scan
  • The Role of Renin-Angiotensin System in Acute Lung Injury and Acute Respiratory Dysfunction Syndrome

    Objective To explore the role of renin-angiotensin system( RAS) in acute lung injury( ALI) /acute respiratory dysfunction syndrome( ARDS) by using amouse cecal ligation and puncture ( CLP)model.Methods The ALI/ARDS animal models were assessed bymeasuring blood gas, wet/dry lung weight ratio( W/D) , and lung tissue histology 18 hours after CLP operation. After the ALI/ARDS models was successfully established, immunohistochemistry, western blotting and radioimmunity were used to investigate the changes of several key enzymes of RAS, such as ACE, ACE2 and Ang Ⅱ. In addition, two groups of animals received a separate intraperitoneal injection of angiotensin-converting enzyme ( ACE) inhibitor captopril or recombinant mouse ACE2 ( rmACE2) after CLP, then the changes of RAS in ALI/ARDS modelswere observed. Results The extensive lung injuries can be observed in the lung tissues from CLP-treated animals 18 hours after operation. The CLP-induced ALI/ARDS led to an increase in the wet/dry weight ratio of the lung tissues, and a decrease in the PaO2 /FiO2 [ ( 194. 3 ±23. 9) mm Hg vs ( 346. 7 ±20. 5) mm Hg,P lt;0. 01] . Immunohistochemistry and western blotting tests of the lung tissues from CLP-treated animals showed a decrease in the ACE2 protein level. However, in both the CLP and sham mice there were no significant differences between the two groups. CLP markedly increased Ang Ⅱ level in lungs and plasma of mice, and RAS drugs significantly impacted the Ang Ⅱ levels of mice. Compared with the CLP group,captopril or rmACE2 led to a decrease of the Ang Ⅱ level in mice [ Lung: ( 1. 58 ±0. 16) fmol /mg,( 1. 65 ±0. 21) fmol /mg vs ( 2. 38 ±0. 41) fmol /mg; Plasma: ( 178. 04 ±17. 87) fmol /mL, ( 153. 74 ±10. 24) fmol /mL vs ( 213. 38 ± 25. 44) fmol /mL] . Conclusions RAS activation is one of the characteristics of CLP-induced ALI/ARDS in mice models. ACE and ACE2 in RAS have a different role in the regulation of AngⅡ synthesis, while ACE has a positive effect in generating AngⅡ, and ACE2 shows a negative effect.

    Release date:2016-08-30 11:53 Export PDF Favorites Scan
  • Losartan Alleviates Lung Inflammation of Rats with Acute Lung Injury

    Objective To investigate the role of angiotensin-II type 1 receptor ( AT1) antagonist in treatment of acute lung injury/acute respiratory distress syndrome ( ALI/ARDS) . Methods Animal model of ALI/ARDS was induced by cecal ligation and perforation ( CLP) . ALI/ARDS animals received a separate intraperitoneal injection of several concentrations( 5, 10, 15, 20, 25 mg/kg) of AT1 inhibitor losartan after CLP, then the changes of lung injury and 7-day survival were measured. Results Oxygenation index and lung wet to dry weight ratio ( W/D) showed an improving trend when losartan was administered at doses of 5 to 15 mg/kg in ALI/ARDS rats, but aggravated above the dose of 15 mg/kg. Losartan ( 15 mg/kg) treatment significantly alleviated pulmonary edema after CLP operation, and decreased serumlevels of TNF-α, IL-6, andIL-1β [ TNF-α: ( 554. 1 ±62. 7 ) pg/mL vs. ( 759. 2 ±21. 5 ) pg/mL, P lt; 0. 01; IL-6: ( 1227. 3 ±130. 0) pg/mL vs. ( 2670. 4 ±174. 1) pg/mL, P lt; 0. 01; IL-1β: ( 444. 0 ±38. 6) pg/mL vs. ( 486. 6 ±61. 7)pg/mL, P lt; 0. 05] . 7-day survival rate also increased in losartan treatment group at a dose of 15 mg/kg( 6. 7% vs. 0 ) . Conclusions The AT1 inhibitor, losartan, can significantly prevent lung injury in ALI/ARDS after CLP, and improve the 7-day survival rate.

    Release date:2016-08-30 11:53 Export PDF Favorites Scan
  • 先天性心脏病合并肺动脉高压患者血浆血管紧张素Ⅱ的变化及意义

    目的 观察先天性心脏病合并肺动脉高压患者术前血浆血管紧张素的变化,探讨其在先天性心脏病合并肺动脉高压诊治中的意义.方法 根据平均肺动脉压/平均主动脉压(MPAP/MAP)的不同将80例先天性心脏病患者分为4组,每组20例.对照组:MPAP/MAP<0.25;轻度肺动脉高压组(组Ⅰ):MPAP/MAP 0.25~0.45;中度肺动脉高压组(组Ⅱ):MPAP/MAP 0.46~0.75;重度肺动脉高压组(组Ⅲ):MPAP/MAP>0.75.采用放射免疫法测定术前血浆血管紧张素Ⅱ浓度,测定患者术中血流动力学指标.结果 组Ⅰ和组Ⅱ血管紧张素Ⅱ均显著高于对照组(P<0.01);但组Ⅲ中血管紧张素Ⅱ与对照组比较无差异(P>0.05).结论 血管紧张素Ⅱ在先天性心脏病合并肺动脉高压的发病中可能起了一定的作用,围术期应用血管紧张素转换酶抑制剂以降低肺动脉压力,对提高该类患者的手术成功率有一定意义.

    Release date:2016-08-30 06:35 Export PDF Favorites Scan
  • EFFECT OF ANGIOTENSIN Ⅱ ON TRANSFORMING GROWTH FACTOR β-INDUCED FIBROBLAST PROLIFERATION IN HUMAN SKIN

    Objective To observe the effect of angiotensin Ⅱ (Ang Ⅱ) or/and transforming growth factor β(TGF-β) on human skin fibroblast proliferation, and to explore the possible signaling mechanism involved in their actions. Methods Cultured human skin fibroblasts were treated with different concentrations of Ang Ⅱ (1×10-10 , 1×10-9,1×10-8 and 1×10-7 mol/L) , TGF-β(0.1, 1.0 and 10.0 ng/ml), and 1×10 -10 mol/L Ang Ⅱ+0.1 ng/ml TGF-β, respectively. The cell proliferation was determined by3Hthymidine (3H-TdR) incorporation. The phosphorylation of extracellular signalregulated kinases (ERK) was detected by Western blot. Results Ang Ⅱ at 1×10-9,1×10-8,1× 10-7 mol/L or TGF-β at 1.0, 10.0 ng/ml increased 3H-TdR incorporation into cultured skin fibroblasts dose-dependently. Ang Ⅱ and TGF-β at lower doses (1×10-10 mol/L and 0.1 ng/ml, respectively) did not affect 3H-TdR incorporation into fibroblasts (Pgt;0.05), whereas co-administration of both Ang Ⅱ and TGF-β at these doses significantly increased 3H-TdR incorporation intofibroblasts(Plt;0.05). Ang Ⅱ at 1×10-7 mol/L or TGF-β at 10.0 ng/ml significantly increased ERK phosphorylation of fibroblasts after stimulation (Plt;0.01). Smaller doses of Ang Ⅱ (1×10-10 mol/L) or TGF-β (0.1 ng/ml) did not influence ERKphosphorylation of fibroblasts, whereas co-administration of Ang II and TGF-β at these doses significantly enhanced ERK phosphorylation (Plt;0.05). Total protein levels of ERK did not differ at different doses. Conclusion These results indicate that Ang Ⅱ and TGF-β synergistically increase skin fibroblast proliferation, which is at least partly via enhancement of ERK activity.

    Release date:2016-09-01 09:26 Export PDF Favorites Scan
  • 肾素-血管紧张素系统阻滞剂预防早产儿视网膜病变研究

    血管紧张素Ⅱ(Ang Ⅱ)是肾素血管紧张素系统(RAS)的主要效应产物和多种器官有效的生长因子。在早产儿视网膜病变(ROP)等缺血性视网膜病变中,RAS上调,视网膜RAS被激活,刺激具有促微血管渗漏、周细胞迁移、新生血管生成和纤维化功能的血管内皮生长因子(VEGF)等上调。对RAS的阻滞主要通过血管紧张素转换酶抑制剂和血管紧张素Ⅱ受体拮抗剂来实现。RAS阻滞剂在ROP的发生发展过程中可能具有防止和减弱病理性血管生成的作用。对RAS的阻断有望成为ROP的治疗途径。

    Release date:2016-09-02 05:41 Export PDF Favorites Scan
  • 他汀类药物和血管紧张素Ⅱ受体拮抗剂治疗慢性阻塞性肺疾病的研究

    慢性阻塞性肺疾病(COPD)以气道、肺实质和肺血管的慢性炎症为特征,近年来发现他汀类药物除降脂作用外,还可改善COPD患者的症状及预后。血管紧张素Ⅱ受体拮抗剂,能抑制肺血管缺氧性收缩以及慢性缺氧时血管的重建。能防止COPD患者肺动脉高压的病程进展及肺功能的下降。两者合用有协调作用,不仅能缓解COPD患者的症状,还能延缓COPD的进程,降低死亡率。

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  • Effects of Angiotensin Ⅱ Receptor Blocker on P Wave Deviation Degree in Patients with Paroxysmal Atrial Fibrillation

    目的:探讨血管紧张素Ⅱ受体拮抗剂(ARB)对PAF患者P波离散度的影响。方法:观察48 例阵发性AF患者的最宽P 波和P 波离散度,并与ARB干预治疗3 个月后进行对比分析。结果:ARB治疗3个月后最宽P波、P 波离散度及P 波离散度≥40 ms的例数与治疗前比较差异有统计学意义 (Plt;0.05或lt;0.01)。结论:ARB能减轻PAF患者心房结构重构及电重构,减少AF的发生。

    Release date:2016-09-08 10:00 Export PDF Favorites Scan
  • Mitochondria Mediates Induction of NOX1 Gene Expression by AngⅡ

    摘要:目的: 探讨在血管紧张素Ⅱ(AngⅡ)诱导血管平滑肌细胞(VSMCs)NOX1基因表达增加中线粒体所起的作用。 方法 :体外培养大鼠主动脉VSMCs,用线粒体呼吸链的抑制剂阻断线粒体的作用,用荧光实时定量PCR检测NOX1基因表达的量。 结果 :AngⅡ能够诱导 NOX1基因的表达增加,线粒体呼吸链的抑制剂能够抑制上述这一作用。 结论 :在大鼠的VSMCs中,AngⅡ诱导NOX1的增加通过线粒体呼吸的作用。Abstract: Objective: To detect the role of mitochondria involved in Angiotensin Ⅱ(Ang Ⅱ) induced NOX1 gene expression. Methods :Rat aortic vascellum smooth muscle cells(VSMCs) were cultured in vitro,and were treated with or without some inhibitors of complexs in mitochondrial respiratory chain. Realtime RTPCR was used to calculate the expression of NOX1 mRNA. Results :AngⅡ stimulated NOX1 gene expression,while some inhibitors of complexs in mitochondrial respiratory chain attenuated this progress.〖WTHZ〗Conclusion : Mitochondrial respiratory chain mediates expression of NOX1 gene in VSMCs by AngⅡ.

    Release date:2016-09-08 10:12 Export PDF Favorites Scan
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