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体外研究表明:血管紧张素Ⅱ(AngⅡ)可引起心肌细胞肥大,但其信息传递途径尚不清楚。本文通过^3H-Leu掺入率的测定与RNA狭线杂交技术,初步探讨了AngⅡ受体、Ca^2+及蛋白激酶C(PKC)在AugⅡ刺激乳鼠心肌细胞蛋白质合成中的作用,并观察了AngⅡ对原癌基因c-fos表达的影响。结果发现,培养液中加入钙通道阻断剂-Verapamil、细胞外钙螯合剂-EGTA、肌浆网钙释放抑制剂-Dant 相似文献
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血管紧张素Ⅱ对心肌梗塞后心肌细胞核酸,蛋白质合成… 总被引:1,自引:0,他引:1
通过分离、培养心肌梗塞后成年大鼠的心肌细胞(MC),观察了血管紧张素Ⅱ(AngⅡ)在不同处理因素对照下,对MC核酸、蛋白质合成的影响。结果显示:在相同浓度的AngⅡ(10^-7M)作用下,MI组MC的RNA和蛋白质的合成速率均显著高于假手术组(p〈0.05)。 AngⅡ的上述作用,可分别被AT1受体阻滞剂Losarta n、特异性AngⅡ拮抗剂^〔1,3〕AngⅡ和血管紧张素抗肽(Amg-AP)PF 相似文献
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血管紧张素Ⅱ受体研究进展 总被引:1,自引:0,他引:1
肾素-血管紧张素系统在维持水、电解质平衡及调节血压中起着关键的作用。血管紧张素Ⅱ是肾素-血管紧张素系统中最重要的介质,与其特异性受体结合,对心脏和血管功能、结构产生显著影响。近年来,人们对血管紧张素Ⅱ的分型、分子特征、生物学功能、信号转导及其基因多态性的研究不断深入。本文就血管紧张素Ⅱ受体在心血管系统中的研究进展予以综述。 相似文献
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肾素血管紧张素系统(RAS)在血压调节机制中起着极为重要的作用,多年来人们致力于寻找有效的血管紧张素受体(AT)拮抗剂,以期在受体水平阻断RAS。有关血管紧张素受体的研究工作相当迟缓,其原因是作为主要工具药的肽类AugⅡ类似物虽有抬抗剂作用,可总是残留着部分的激动剂,且作用时间十分短暂。近年来,应用分子生物学技术对血管紧张素受体进行分子克隆和氨基酸测序,成功地制备出具有高度选择性而无激动剂活性的非肽类AugⅡ拮抗剂-Losartan.1AngⅡ受体的分型、分布和特点:在药理学上根据对配体结合特性的不同将AugⅡ受体分为A… 相似文献
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目的:评价转染AT1反义核苷酸(AT1A)对心肌细胞血管紧张素Ⅱ(AngⅡ)受体亚型mRNA表达,及蛋白质和核酸合成的作用。方法:RT-PCR克隆AT1 cDNA序列(476bp),将克隆的AT1 cDNA反向插入PcDNA3.1(5.4kb),构建一完整的含AT1A的质粒(PAT1A),并转染入培养的心肌细胞,RT-PCR和免疫印迹鉴定其转染后AT1 mRNA和蛋白表达。比较AngⅡ10^-7 mol/L刺激24h后的转染及非转染的心肌细胞AT1及AT2 mRNA表达(RT-PCR)、蛋白质和核酸合成(^3H-Leu及^3H-TdR掺入量)。结果:成功构建PAT1A。转染心肌细胞AT1mRNA和蛋白表达量显著减少,与正常对照心肌细胞相比差异有非常显著性(P<0.01)。AngⅡ10^-7mol/L刺激24h后,与非转梁心肌细胞相比,转染组AT1 mRNA表达明显减少,AT2 mRNA表达明显增加(P<0.01),但两组间^3H-Leu及^3H-TdR掺入量差异均无显著性(P>0.05)。结论:经AT1A封闭后,心肌细胞AT1mRNA表达显著抑制,同时AT2 mRNA上调。单纯封闭AT1mRNA并不能有效阻断AngⅡ介导的心肌细胞生长。 相似文献
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血管紧张素Ⅱ是肾素-血管紧张素系统中主要活性肽,其中起主要作用的受体为AT1和AT2.血管紧张素Ⅱ受体拮抗剂是继血管紧张素转换酶抑制剂后又一类抗高血压药物,主要通过阻断AT1受体起作用,其不但具有强大而持久的降压效果,还具有靶器官保护作用. 相似文献
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近年来,血管紧张素Ⅱ受体作为抗肿瘤药物的靶点越来越受到重视,国内外对血管紧张素Ⅱ受体进行了深入研究,发现血管紧张素Ⅱ受体在很多肿瘤中过表达,进一步研究揭示,许多肿瘤的生长与血管紧张素Ⅱ受体密切相关,作者就此作一综述。 相似文献
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高血压是一种以动脉血压升高为特征,可伴有心脏、血管、脑和肾脏等器官功能性或器质性改变的全身性疾病,严重影响患者的身体健康和生命质量。血管紧张素2(AngⅡ)受体是肾素一血管紧张素系统(RAS)的主要活性介质,在高血压及其靶器官损害中起重要病理生理作用。随着AngⅡ受体的克隆和非肽类AngⅡ型(AT1)受体拮抗剂的问世,使受体水平拮抗循环和局部AngⅡ的作用成为目前治疗高血压的新观念和新方法。受体拮抗剂种类较多,其基本药理作用相同,都是通过与AT1受体特异性结合而拮抗AngⅡ的升血压和损害靶器官作用。现就AT1受体及其拮抗剂的研究和临床应用作一综述。 相似文献
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Effect of angiotensin Ⅱ and angiotensin Ⅱ type 1 receptor antagonist on the proliferation,contraction and collagen synthesis in rat hepatic stellate cells 总被引:11,自引:0,他引:11
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
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
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观察了酮替芬(Ket)对新生鼠心肌细胞内游离钙的影响,以酶法制备新生大鼠心肌细胞悬液,用荧光探针Fura-2/AM检测心肌细胞内游离钙浓度的变化。结果表明:Ket对静息状态下「Ca^2+」i无影响,Ket(10 ̄500μmol/L)剂量依赖性抑制高钾去经及NE所致的「Ca^2+」i升高。提示:Ket对心肌细胞膜下坟依赖性钙通道有抑制作用,也可能抑制受体操纵型钙通道。 相似文献
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目的 观察二甲双胍对内皮细胞1型血管紧张素II受体(AT1R)表达的影响并探讨其机制。方法 应用western-blot检测内皮细胞AT1R、腺苷酸活化蛋白激酶α亚基(AMPKα)、核转录因子κB抑制蛋白(I-κB)的表达,应用激光共聚焦观察核转录因子κB(NF-κB )P65 在细胞核内变化,比色法测定各组内皮细胞培养液乳酸脱氢酶(LDH)活性。同时应用RNA干扰技术,进一步观察I-κB 、AMPKα的作用。结果 二甲双胍显著减少肿瘤坏死因子α(TNFα)诱导的内皮细胞AT1R的蛋白表达(P<0.01),显著降低I κB的磷酸化(P<0.01),同时二甲双胍显著降低内皮细胞培养液LDH活性(P<0.01),而AMPKαSiRNA干预后,二甲双胍对内皮细胞AT1R的影响作用显著减弱(P<0.01)。结论 二甲双胍通过促使AMPKα磷酸化,激活AMPKα信号通路,抑制NF-κB活化和内皮细胞AT1R的表达,减轻内皮细胞损伤,保护内皮细胞功能,从而发挥其对心血管的有益作用。 相似文献
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OBJECTIVE: To investigate the role of mitogen-activated protein kinase (MAPK) in the regulation of cyclin-dependent kinase inhibitors (CDKI) in the process of vascular smooth muscle cell (VSMC) hypertrophy induced by angiotensin II stimulation. METHODS: The medial layer of male SD rat aorta was isolated for VSMC culture. After cultured in serum-free medium to arrest the cell growth, VSMCs were stimulated with angiotensin II (1x10(-6) mol/L) or/and phorbol myristate acetate (PMA, 20 nmol/L), with the cells cultured in serum-free medium serving as control. MAPK activity of the cells was assayed 90 min after stimulation with immunoprecipitation test, and the expression levels of CDKI p27, p57 and p21 were determined by Western blotting 6 and 24 h after stimulation respectively. RESULTS: Compared with the control level, MAPK activity of the VSMCs was up-regulated by 238% by treatment with angiotensin II alone which, however, did not inhibit p27 expression or induce VSMC proliferation. Costimulation with angiotensin II and PMA slightly inhibited p27 expression but VSMC proliferation was still not observed. CONCLUSION: MAPK pathway is an important channel for extracellular proliferative and hypertrophic signal transduction into the nucleus of VSMCs. 相似文献
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Effect of valsartan-eluting stents on the expression of angiotensin Ⅱ type 2 receptor 总被引:7,自引:0,他引:7
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
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《中华医学杂志(英文版)》2006,119(7):601-604
Percutaneous coronary intervention (PCI) with drug-eluting stent implantation has been proved efficient 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… 相似文献
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目的 :探讨血管紧张素II在不同浓度和不同作用时间下对血管内皮细胞凋亡的作用及卡托普利和氯沙坦的影响。方法 :采用流式细胞术测定在血管紧张素II不同浓度和不同作用时间下血管内皮细胞凋亡率的变化和卡托普利、氯沙坦的影响。结果 :血管紧张素II可明显促进血管内皮细胞凋亡 ,且其作用呈剂量依赖性和时间依赖性 ;单用氯沙坦对细胞凋亡无明显作用 ,卡托普利有一定的作用 ,二者合用时抑制作用较明显。结论 :血管紧张素II具有明显的促血管内皮细胞凋亡的作用 ;合用卡托普利和氯沙坦可明显抑制内皮细胞凋亡 相似文献
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氯沙坦、福辛普利对高血压大鼠心肌纤维化、血管紧张素Ⅱ及左室重构的影响 总被引:6,自引:0,他引:6
目的:评价氯沙坦、福辛普利对自发性高血压大鼠(SHR)心肌纤维化=、左室重构及血浆和心肌组织中血管紧张素Ⅱ的效应。方法:16周龄SHR随机分为3组,即氯沙坦治疗组(SHR-L组)、福辛普利治疗组(SHR-F组)、空白对照组(SHR-C组),每组各10只。分别采用病理检查及放射免疫测定方法对治疗8周、16周的SHR心肌胶原容积分数(CVF)和心肌血管周围胶原面积(PVCA)、血浆和组织中血管紧张素Ⅱ进行检测。结果:在治疗8周、16周后,两治疗组的收缩压较对照组均有明显下降;治疗组组间比较差异无显著性(P>0.05);心脏重量(HW)、心脏重量指数(HWI)、左室重量(LVW)、左室重量指数(LVMI)均有显著性改善,且治疗16周后SHR-F组较SHR-L组LVMI显著性降低(P<0.05)。两治疗组CVF和PVCA与对照组比较明显下降(P<0.01)。治疗16周后SHR-F组CVF较SHR-L组下降更明显。SHR-L组血浆及心肌组织中AngⅡ显著增加,而SHR-F组心肌组织AngⅡ显著下降,但对血浆AngⅡ无明显影响。结论:氯沙坦、福辛普利均能有效逆转心脏肥厚及抗心肌纤维化,以福辛普利作用显著。其作用机制可能与拮抗心肌组织中肾素-血管紧张素-醛固酮系统(RAS)效应有关。 相似文献
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目的 观察组胺对脑细胞内游离钙浓度的影响,并初步探讨其作用机制。方法 利用荧光探针Fura-2测定乳鼠脑细胞内游离钙的浓度。结果 组胺可明显升高脑细胞内游离钙浓度,而异丙嗪可以阻断组胺的这一效应。结论 组胺升高脑细胞内游离钙浓度是由H1受体介导的。 相似文献