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1.
EFFECTS OF CERTAIN VASOACTIVE PEPTIDES ON PATHOGENESIS OF VASCULAR RESTENOSIS   总被引:13,自引:0,他引:13  
Objective. To investigate the effects of several vasoactive peptides on the development of arterial restenosis after balloon angioplasty.Methods. In rat aortic artery restenosis model produced by denudation of aortic endothelia, we observed changes of endothelin (ET), angiotensin II (AII), calcitonin gene-related peptide (CGRP) and adrenomedullin (Adm) in plasma and aorta with radioimmunoassay and expression of hypertension-related gene (HRG-1) with semi-quantitative RT-PCR, and studied the effects of these peptides on intimal hyperplasia, intima/media ratio and MAPK activities of aortic artery after angioplasty respectively. Furthermore, in cultured cells, we studied the effects of these peptides on vascular smooth muscle cell (VSMC) proliferation and expression of HRG-1 of VSMC from spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats with 3H-TdR incorporation and RT-PCR respectively.Results. After angioplasty, the levels of ET and AII in plasma and aorta significantly increased, accompan  相似文献
2.
Background Angiotensin Ⅱ (Ang Ⅱ) is a very important vasoactive peptide that acts upon hepatic stellate cells (HSCs), which are major effector cells in hepatic cirrhosis and portal hypertension. The present study was aimed to investigate the effects of Ang Ⅱ and angiotensin Ⅱ type 1 receptor antagonist (AT1RA) on the proliferation, contraction and collagen synthesis in HSCs.
Methods HSC-T6 rat hepatic stellate cell line was studied. The proliferation of the HSC cells was evaluated by MTT colorimetric assay while HSC DNA synthesis was measured by ^3H-thymidine incorporation. The effects of angiotensin Ⅱ and AT1RA on HSCs contraction were studied by analysis of the contraction of the collagen lattice. Cell culture media were analyzed by RT-PCR to detect secretion of collagen Ⅰ (Col Ⅰ), collagen Ⅲ (Col Ⅲ) and transforming growth factor β1 (TGF-β1) by enzyme linked immunosorbent assay. HSC was harvested to measure collagen Ⅰ, collagen Ⅲ and tissue inhibitor of metalloproteinase-1 (TIMP-1) mRNA expression.
Results Ang Ⅱ ((1×10^-10-1×10^-4)mol/L)stimulated DNA synthesis and proliferation in HSCs compared with untreated control cells. AT1RA inhibited angiotensin Ⅱ induced proliferation of HSCs. A linear increase in the contractive area of collagen lattice correlated with the concentration of angiotensin Ⅱ (1×10^-9-1×10^-5 mol/L) and with time over 48 hours. AT1RA blocks angiotensin Ⅱ induced contraction of collagen lattice. Col Ⅰ, Col Ⅲ and TGF-β1 levels of the Ang Ⅱ group were higher than those of control group and this increase was downregulated by AT1RA. The mRNA expressions of Col Ⅰ, Col Ⅲ and TIMP-1 were higher in HSCs from the Ang Ⅱ group than the control group and downregulated by AT1RA.
Conclusions Angiotensin Ⅱ increased DNA synthesis and proliferation of HSCs in a dose-dependent manner, stimulated the contraction of HSCs dose- and time-dependently. Angiotensin also promoted excretion of Col I, Col Ⅲ and TGF-β1 lev  相似文献
3.
目的 观察血管紧张素Ⅱ (AngⅡ )和血小板源生长因子BB(PDGF BB)对血管平滑肌细胞和心肌细胞中细胞周期素和P2 7蛋白表达量的不同影响。方法 培养的血管平滑肌细胞或乳鼠心肌细胞 ,加入AngⅡ 10 -6 mol/L、PDGF BB 2 0ng/ml后 2 4小时收集细胞 ,用碘化丙啶 (PI)标记细胞DNA ,以确定细胞所处的周期。用细胞周期素 (CyclinD、CyclinE、CyclinA)或P2 7蛋白的单克隆抗体和标记FITC的二抗标记细胞 ,用流式细胞仪测定被激发出的荧光量来测定细胞周期素和P2 7蛋白表达的相对量。结果 AngⅡ除轻度增加心肌细胞CyclinE表达 ( 2 3 9± 4 3对照 8 9± 1 6,P <0 0 1)外 ,对 2种细胞中其他细胞周期素和P2 7蛋白的表达没有明显影响 ,不能促进血管平滑肌细胞和心肌细胞增殖 ;PDGF BB可明显促进 2种细胞中细胞周期素的表达 ,抑制血管平滑肌细胞中P2 7的表达 ( 1 8±1 3、对照 4 8 1± 5 4 ,P <0 0 1) ,但不能抑制心肌细胞P2 7的表达 ( 3 9 4± 5 6、对照 4 4 6± 3 6,P >0 0 5 ) ,因而仅能促进血管平滑肌细胞增殖 ,却不能促进心肌细胞增殖。结论 P2 7蛋白是血管平滑肌细胞和心肌细胞能否进入细胞周期并进行有丝分裂的重要调节因子。  相似文献
4.
Peng J  Peng S  Gong W 《中华医学杂志》2002,82(7):471-473
目的:研究血管紧张素Ⅱ-1型受体(AT1R)基因A1166/C多态性与中国早发冠心病(CHD)发生的相关关系及其对血脂水平的影响。方法:采用聚合酶链反应一限制性片段长度多态性(PCR-RFLP)分子生物学方法,检测71例早发CDH患者,76例迟发CHD患者和119例健康对照者的AT1R基因型;并按常规方法测定血脂水平。结果:共检测出2种AT1R基因型,分别是AA型和AC型,早发CHD组及迟发CHD组AA基因型(97.2%,92.1%)和AC基因型(2.8%,7.9%)频率与对照组(94.1%,5.9%)相比差异均无统计学意义。等位基因A和C频率在3组间差异无显著意义。AT1R基因多态性与血脂水平无关。结论:AT1R基因A1166/C多态性与早发CHD的发生发展似无直接关系。  相似文献
5.
MAPKs阻断剂对乳鼠心肌细胞能量代谢的影响   总被引:5,自引:0,他引:5  
目的 :在原代培养的心肌细胞上观察分裂酶原激活的蛋白激酶系统 (MAPKs)特异阻断剂PD0 980 5 9对心肌细胞活力与增殖能力的影响 ,旨在探讨细胞内信号传递通路的阻断是否能有效地干预细胞能量代谢 ,为寻找新的心衰预防与治疗药物提供实验依据 .方法 :利用培养的乳鼠心肌细胞 ,根据活细胞线粒体在能量代谢过程中可作用于MTT产生蓝紫色结晶产物formazan这一原理 ,应用比色法测定血管紧张素Ⅱ (AngⅡ )对培养心肌细胞的活力的影响和PD0 980 5 9的干预作用 .结果 :AngⅡ在 12h内使formazan产物的值逐渐上升 ,12h达到高峰 (A值 :0 .36 4 3± 0 .0 2 4 1) ,此后开始下降 ,至2 4h已低于正常水平 (A值 :0 .2 785± 0 .0 912 ) ,它们的值之间均有显著性统计学差异 (P <0 .0 5或 0 .0 1) ,PD0 980 5 9可以显著地拮抗AngⅡ对心肌细胞活力的影响 .结论 :PD0 980 5 9可以显著地拮抗AngⅡ对心肌细胞活力的影响  相似文献
6.
Percutaneous coronary intervention (PCI) with drug-eluting stent implantation has been provedefficient to reduce complications and restenosis in type B2/C lesions compared with bare stent, since the major drawback of the latter technique is intimal hyperplasia from the vessel media, which significantly cause in-stent restonosis. Despite the beneficial effects on the renin-angiotensin-aldosterone (RAAS) system, the role of angiotensin-converting enzyme (ACE) inhibitors after PCI is still unclear. However, first results of angiotensin receptor antagonist (valsartan) after stent implantation in the VaI-PREST1 and VALVACE2 trials have indicated the systemic pharmacological effect in the prevention of in-stent-restenosis. Up to our knowledge, whether local treatment of valsartan by implanting drug-eluting stent can generally prevent restenosis by inhibiting intimal hyperplasia has not been explored.  相似文献
7.
Background Transforming growth factor (TGF) β(1)-Smads signal plays an important role in cardiac remodeling following myocardial infarction (MI). In addition, both angiotensin converting enzyme inhibitor (ACEI) and angiotensin II type I receptor blocker (ARB) can effectively prevent left ventricular remodeling. The current study focused on whether the combination of ACEI and ARB is more beneficial for preventing ventricular remodeling and whether Smad proteins mediate this beneficial effect.Methods MI was induced by ligating the left anterior descending coronary artery in rats. Twenty-four hours after ligation, the survived rats were randomly divided into five groups and treated for 8 weeks: placebo group, ACEI group (benazepril 10 mg·kg(-1)·d(-1)), ARB group (irbesartan 50 mg·kg(-1)·d(-1)), ACEI+ARB group (benazepril 10 mg·kg(-1)·d(-1)+irbesartan 50 mg·kg(-1)·d(-1)) and control group (sham-operated rats). After 8 weeks, we examined the following indexes: the ratio of ventricular weight to body weight (VW/BW), left ventricular end diastolic dimension (LVDd), ejection fraction (EF), fractional shortening (FS), ratio of E-wave to A-wave velocity, collagen of noninfarcted zone, the mRNA expression of TGFβ(1), Smad 2, and Smad 3 by RT-PCR in noninfarcted zone, the protein expression of Smad 2 and Smad 3 in noninfarcted zone by Western blot.Results VW/BW significantly increased in the placebo groups compared with that in the control group (P&lt;0.01). This increase was limited in ACEI, ARB, and combined groups (P&lt;0.01 compared with placebo group). There was no significant difference among the three actively treated groups. Collagen was increased in placebo group (5.68±0.5)% compared with that in control group (P&lt;0.01). ACEI, ARB and combined treatment attenuated this increase of collagen [(4.3±0.5)%, (3.5±0.5)%, (3.2±0.4)%] in comparison with that in placebo group (P&lt;0.01 respectively). Combined treatment showed more significant effect on collagen deposition. EF and FS significantly decreased, LVDd and E/A significantly increased in placebo group compared with that in control group (P&lt;0.01 respectively). ACEI, ARB and combined treatment ameliorated these indexes (P&lt;0.01 compared with placebo group). The mRNA expression of TGFβ(1), Smad 2, and Smad 3 (0.700±0.045, 0.959±0.037 and 0.850±0.051) increased in placebo group compared with that in control group (P&lt;0.01). ACEI, ARB and combined treatment normalized the increase (P&lt;0.01). Furthermore, ARB and combined treatment proved to be more effective in decreasing TGF β(1) and Smad mRNA expression than ACEI treatment (P&lt;0.01). The expression of Smad 2 and Smad 3 protein increased in placebo group compared with that in control group (P&lt;0.01). ACEI, ARB and combined treatment normalized the increase (P&lt;0.01). Furthermore, ARB and combined treatment proved to be more effective than ACEI alone (P&lt;0.01).Conclusions TGFβ(1)-Smads signal activation is correlated with ventricular remodeling following MI. ACEI and ARB treatment prevents ventricular remodeling by inhibiting expression of Smad 2 and Smad 3. ARB and combined treatment are more effective than ACEI alone.  相似文献
8.
袁侨英  覃数 《重庆医学》2005,34(1):66-67
目的在大鼠结扎前降支致心肌梗死的模型上观察辛伐他汀抑制血管紧张素Ⅱ(AngⅡ)及AngⅡ诱导的活性氧(H2O2)生成,是否有利于改善心室重塑和心功能的作用.方法结扎大鼠冠状动脉前降支造成心肌梗死模型,给予辛伐他汀干预.8周后,测定心脏重量指数、血流动力学指标、血液及心肌中AngⅡ含量,血液过氧化氢(H2O2)含量,并与假手术组比较. 结果心肌梗死组(M组)大鼠右室重量指数(RVWI)、左室重量指数 (LVWI)升高(P<0.01),外周动脉压(APS)、舒张压(APD)均降低,(P<0.01).左室收缩压(LVSP)和心室收缩期室内压上升速率( dp/dtmax),心室舒张期室内压下降速率(-dp/dtmax)下降(P<0.01),左室舒张末压( LVEDP)升高(P<0.01).心肌、血液中AngⅡ含量升高(P<0.01);H2O2含量升高 (P<0.01).辛伐他汀干预组较M组辛RVWI、 LVWI下降(P<0.01),APS、APD、LVSP、 dp/dtmax、-dp/dtma均回升(P<0.01),LVEDP回落(P<0.01);心肌、血液中AngⅡ含量下降(P<0.01),H2O2含量下降(P<0.01).结论辛伐他汀抑制急性心肌梗死后血管紧张素Ⅱ(AngⅡ)及AngⅡ诱导的H2O2生成,可能是改善心室重塑和心功能的机制之一.  相似文献
9.
10.
Summary The model of hypertensive rat was established by using the method of abdominal aortic constriction. 33 male SD rats were randomly divided into 4 groups: group A (sham-operated rats serving as controls), group B (hypertensive rats serving as controls), group C (hypertensive rats subjected to low-dose perindopril treatment, 0. 1 mg· kgt-1d) and group D (hypertensive rats receiving high-dose perindopril treatment, 1. 5 mg· kgt-1d). The drug was administered by gavage for 4 weeks. At the end of the treatment, mean arterious pressure (MAP) was measured via catheter in the carotid artery. The heart was taken and weighed to calculate the ratio of left ventricular weight to body weight (LVW/ BW). The ratio of medial mean thickness to mean diameter of lumen of aorta and superior mesenteric artery was calculated by morphometry. Concentration of angiotensin II (A II) in plasma and in aortic wall were determined by radioimmunoassay (PA II, AA II. Our results showed that both high-dose and low-dose perindopril may prevent hypertrophy of left ventricle and hypertrophy of the tunica media of superior mesenteric artery. In addition, high-dose perindopril may significantly inhibit hypertrophy of aortic media. The above effects of perindopril may be explained by inhibition on tissue renin-angiotensin system of both vascular wall and heart, but is not related to circulating A II (PA II).  相似文献
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