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益脉降压流浸膏对老年原发性高血压患者肾上腺髓质素、内皮素及血管紧张素Ⅱ的影响(英文)

中国临床康复 2004年第30期8卷 6808-6810页

作者：段学忠孙西庆蔡新吉张燕解放军济南军区总医院中医科山东省济南市250031 山东中医药大学附属医院内科山东省济南市250011

背景:原发性高血压患者血浆肾上腺髓质素(adrenomedullin,ADM)、内皮素、血管紧张素Ⅱ(angiotensinⅡ,AngⅡ)水平升高,但抗高血压治疗对其影响尚未十分了解。目的:探讨益脉降压流浸膏对老年气虚血瘀证型Ⅱ期原发性高血压患者血管活性物... 详细信息

背景:原发性高血压患者血浆肾上腺髓质素(adrenomedullin,ADM)、内皮素、血管紧张素Ⅱ(angiotensinⅡ,AngⅡ)水平升高,但抗高血压治疗对其影响尚未十分了解。目的:探讨益脉降压流浸膏对老年气虚血瘀证型Ⅱ期原发性高血压患者血管活性物质的影响。设计:以诊断为依据,随机对照试验。地点、对象和方法:病例来源于济南军区总医院及山东中医药大学附属医院,实验在山东中医药大学附属医院中心实验室进行。入选的60例患者均系1999-03/09期间观察的患者,其中住院患者36例,门诊患者24例。纳入标准:年龄≥60岁,符合1993年WHO/ISH高血压诊断标准,排除标准:排除继发性高血压、糖尿病、冠心病、肝肾疾病及内分泌疾病,剔除Ⅰ期和Ⅲ期原发性高血压,同时按中国中西医结合研究会制定的中医虚证辨证标准及血瘀证诊断标准辨证为气虚血瘀证型者,按随机数字法分为两组。治疗组(益脉降压流浸膏治疗)30例,男17例,女13例;对照组(卡托普利治疗)30例,男18例,女12例。另设健康对照组25例,为同期来济南军区总医院的健康体检者,并为自愿受试者,男14例,女11例。采用放射免疫法测定60例老年气虚血瘀证型Ⅱ期原发性高血压患者治疗前后及25例老年健康人(健康对照组)血浆ADM、内皮素、AngⅡ水平进行比较。结果:治疗组和对照组患者治疗前血?

关键词：高血压/中药疗法膏剂气虚血瘀肾上腺髓质素/代谢内皮素/代谢血管紧张素ⅱ/代谢

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老年血管紧张素Ⅱ和肾素活性的研究：附80例分析

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中国老年学杂志 1986年第1期 51-53页

作者：许凤芝沈阳军区总医院

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张力性头痛和血管性头痛与肾素活性及血管紧张素Ⅱ的关系

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中华内科杂志 1984年第4期23卷 229-230+255-256页

作者：郭述苏韩丽华葛树叶解英凡彭立义杨道理济南部队总医院神经科济南部队总医院免疫室

本文对临床最常见的35例张力性头痛和21例血管性头痛患者测定了肾素活性和血管紧张素Ⅱ的水平,并以健康人20例作为对照。结果前两组病人的肾素活性平均值明显高于对照组;血管紧张素Ⅱ在张力性头痛患者平均浓度虽有显著升高,但波动范围很... 详细信息

本文对临床最常见的35例张力性头痛和21例血管性头痛患者测定了肾素活性和血管紧张素Ⅱ的水平,并以健康人20例作为对照。结果前两组病人的肾素活性平均值明显高于对照组;血管紧张素Ⅱ在张力性头痛患者平均浓度虽有显著升高,但波动范围很大,在低血压时显示其极不稳定。

关键词：肾素/代谢头痛/代谢血管紧张素ⅱ/代谢血管性头痛

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房颤患者脑钠素、血管紧张素Ⅱ的变化及氯沙坦的干预作用

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中国误诊学杂志 2008年第14期8卷 3285-3287页

作者：于建华山东枣庄市立医院心内1科山东枣庄277102

目的：探讨房颤患者脑钠素、血管紧张素Ⅱ的变化及氯沙坦在房颤中的治疗价值。方法：入选患者分为对照组（窦律）40例、永久性房颤组46例、阵发性房颤组40例。阵发性房颤组服用可达龙及氯沙坦,永久性房颤组服用氯沙坦及钙离子拮抗剂控... 详细信息

目的：探讨房颤患者脑钠素、血管紧张素Ⅱ的变化及氯沙坦在房颤中的治疗价值。方法：入选患者分为对照组（窦律）40例、永久性房颤组46例、阵发性房颤组40例。阵发性房颤组服用可达龙及氯沙坦,永久性房颤组服用氯沙坦及钙离子拮抗剂控制室率,分别检测各组治疗前后左心房内径及血清脑钠素、血管紧张素Ⅱ水平,进行对照分析。结果：（1）永久性房颤组血脑钠素（BNP）、肾素（PRA）、血管紧张素（ANG）Ⅱ水平及平均左心房内径（LAD）与对照组比较增加（P〈0.05）;阵发性房颤组血BNP、PRA、ANGⅡ与对照组比较升高（P〈0.05）,LAD与对照组比较有升高趋势,但无统计学意义（P〉0.05）。（2）房颤组血BNP水平与左房内径、血管紧张素Ⅱ浓度明显相关（r分别为0.362,0.294,P〈0.05）。（3）永久性房颤组和阵发性房颤组经氯沙坦干预后血BNP水平降低（P〈0.05）,而血浆PRA、ANGⅡ水平升高（P〈0.05）。（4）氯沙坦干预能提高窦律维持率（P〈0.05）,可降低47%的房颤复发危险（RR=0.45,95%可信区间0.260～0.749,P〈0.05）。结论：房颤患者血脑钠素水平的升高可能与房颤的心房重构有关,氯沙坦可能通过干预房颤的心房重构降低脑钠素水平并降低阵发性房颤的复发。

关键词：心房颤动/代谢/药物疗法利钠肽脑/代谢血管紧张素ⅱ/代谢洛沙坦/治疗应用人类

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肺心病与肺炎患者纤维粘连蛋白和血管紧张素转化酶的观察

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中华内科杂志 1991年第4期30卷 236-236页

作者：吕国平崔德健薛丽波文仲光张均晏鹿正理中国人民解放军第三○四医院

近年来,对血浆纤维粘连蛋白(PFN)在感染、创伤、多脏器衰竭等疾病中的作用和血清血管紧张素转化酶(SACE)在结节病、肺损伤等病变中的作用进行了大量研究,但在肺心病和肺炎病人中同时观察

关键词：肺心病/代谢肺炎/代谢纤连蛋白类/代谢血管紧张素ⅱ/代谢人类

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Na⁺/H⁺ exchange hyperactivity and myocardial hypertrophy:: Are they linked phenomena?

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CARDIOVASCULAR RESEARCH 1999年第3期44卷 462-467页

作者： Cingolani, HE Ctr Invest Cardiovasc RA-1900 La Plata Argentina

Time for primary review 22 days. 1 The Na+/H+ exchanger Intracellular pH (pHi) in the majority of living cells is about 6.8–7.2, considerably more alkaline than that predicted for passive distribution of H+ across the cell membrane. For the average membrane potential and for an extracellular pH of 7.4, a pHi value of 6.4 should be expected if H+ were in electrochemical equilibrium. At such a pHi, metabolism and a variety of other cellular functions would be impaired. The existence of mechanisms extruding H+ (or acid equivalents) can explain the maintenance of pHi well above the equilibrium. The Na+/H+ exchanger (NHE) is one of these mechanisms and plays a central role in the regulation of pHi as well as in the control of cell volume and of intracellular Na+ concentration ([Na+]i). In addition, the exchanger appears to facilitate the induction of cellular growth and proliferation in response to numerous growth factors. The NHE has been found in virtually all living cells and may be phylogenetically one of the most primitive transport systems. The system catalyses the electroneutral exchange of Na+ for H+, with a coupled 1:1 stoichiometry. Under physiological conditions, the inwardly directed Na+ gradient, which is maintained by the activity of the Na+–K+-ATPase and the Na+/Ca2+ exchanger, provides a constant driving force for H+ extrusion. According to the electrochemical transmembrane gradients, the NHE should extrude intracellular H+ in exchange for extracellular Na+ until a pHi far beyond physiological values (8.2–8.5) is obtained. However, at a pHi of around 7.1–7.2 the antiporter extrudes only the protons generated by the intermediate metabolism and those leaking into the cell, so that pHi reaches a steady state value. This pHi at which the NHE is almost quiescent (preventing the rise to non-physiological values) is called “set-point”, and can be shifted to more alkaline pHi values by various stimuli. A prominent feature of this exchanger is that growth factors

关键词：血管紧张素ⅱ/代谢血管紧张素转换酶抑制药/药理学抗高血压药/药理学反向转运物/代谢心脏扩大/代谢红细胞/代谢氢离子浓度高血压/代谢心肌/代谢信号传导/药物作用钠氢反向转运物/代谢动物人类

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Agonist-induced phosphorylation of the angiotensin II (AT_1A) receptor requires generation of a conformation that is distinct from the inositol phosphate-signaling state

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JOURNAL OF BIOLOGICAL CHEMISTRY 2000年第4期275卷 2893-2900页

作者： Thomas, WG Qian, HW Chang, CS Karnik, S Baker Med Res Inst Mol Endocrinol Lab Melbourne Vic 8008 Australia Cleveland Clin Fdn Lerner Res Inst Dept Mol Cardiol Cleveland OH 44195 USA

G protein coupled receptors are thought to isomerize between distinct inactive and active conformations, an idea supported by receptor mutations that induce constitutive (agonist-independent) activation. The agonist-promoted active state initiates signaling and, presumably, is then phosphorylated and internalized to terminate the signal. In this study, we examined the phosphorylation and internalization of wild type and constitutively active mutants (N111A and N111G) of the type 1 (AT(1A)) angiotensin II receptor. Cells expressing these receptors were stimulated with angiotensin II (Ang-II) and [Sar(1),Ile(4),Ile(8)]AngII, an analog that only activates signaling through the constitutive receptors, Wild type AT(1A) receptors displayed a basal level of phosphorylation, which was stimulated by AngII, Unexpectedly, the constitutively active AT(1A) receptors did not exhibit an increase in basal phosphorylation nor was phosphorylation enhanced by AngII stimulation. Phosphorylation of the constitutively active receptors was unaffected by pretreatment with the non-peptide AT(1A) receptor inverse agonist, EXP3174, and was not stimulated by the selective ligand, [Sar(1),Ile(4),Ile(8)]AngII. Paradoxically, [Sar(1),Ile(4),Ile(8)]AngII produced a robust (similar to 85% of AngII), dose-dependent phosphorylation of the wild type AT(1A) receptor at sites in the carboxyl terminus similar to those phosphorylated by AngII, Moreover, internalization of both wild type and constitutive receptors was induced by AngII, but not [Sar(1),Ile(4),Ile(8)]AngII, providing a differentiation between the phosphorylated and internalized states. These data suggest that the AT(1A) receptor can attain a conformation for phosphorylation without going through the conformation required for inositol phosphate signaling and provide evidence for a transition of the receptor through multiple states, each associated with separate stages of receptor activation and regulation. Separate transition states may be a

关键词：氨基酸序列血管紧张素Ⅱ/类似物和衍生物血管紧张素ⅱ/代谢血管紧张素Ⅱ/药理学 CHO细胞仓鼠亚科胞吞作用肌醇磷酸类/代谢磷酰化蛋白质构象受体血管紧张素/激动剂受体血管紧张素/化学受体血管紧张素/代谢信号传导动物

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The protein-tyrosine phosphatase SHP-2 is required during angiotensin II-mediated activation of cyclin D1 promoter in CHO-AT_1A cells

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JOURNAL OF BIOLOGICAL CHEMISTRY 2000年第34期275卷 26349-26358页

作者： Guillemot, L Levy, A Zhao, ZJ Béréziat, G Rothhut, B Univ Paris 06 Lab Signalisat Cellulaire Mediateurs Lipid & Cont CNRS UPRESA 7079 F-75005 Paris France Vanderbilt Univ Sch Med Div Hematol Oncol Nashville TN 37232 USA

Angiotensin II (Ang II) binds to specific G protein-coupled receptors and is mitogenic in Chinese hamster ovary (CHO) cells stably expressing a rat vascular angiotensin II type LA receptor (CHO-AT(1A)). Cyclin D1 protein expression is regulated by mitogens, and its assembly with the cyclin-dependent kinases induces phosphorylation of the retinoblastoma protein pRb, a critical step in G(1) to S phase cell cycle progression contributing to the proliferative responses. In the present study, we found that in CHO-AT(1A) cells, Ang II induced a rapid and reversible tyrosine phosphorylation of various intracellular proteins including the protein-tyrosine phosphatase SHP-2. Ang II also induced cyclin D1 protein expression in a phosphatidylinositol 3-kinase and mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK)-dependent manner. Using a pharmacological and a co-transfection approach, we found that p21(ras), Raf-1, phosphatidylinositol 3-kinase and also the catalytic activity of SHP-2 and its Src homology 2 domains are required for cyclin D1 promoter/reporter gene activation by Ang II through the regulation of MAPK/ERK activity. Our findings suggest for the first time that SHP-2 could play an important role in the regulation of a gene involved in the control of cell cycle progression resulting from stimulation of a G protein-coupled receptor independently of epidermal growth factor receptor transactivation.

关键词： 1-磷脂酰肌醇3-激酶/代谢血管紧张素ⅱ/代谢 CHO细胞催化作用仓鼠亚科细胞周期蛋白D1/遗传学 G1期基因表达调控细胞内信号肽和蛋白质类丝裂原激活蛋白激酶类/代谢启动区(遗传学) 原癌基因蛋白质c-raf/代谢原癌基因蛋白质p21(ras)/代谢受体血管紧张素 1型受体血管紧张素/生物合成受体血管紧张素/遗传学 S期 src同源域动物人类大鼠

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Regulation of calcium-sensitive tyrosine kinase Pyk2 by angiotensin II in endothelial cells - Roles of Yes tyrosine kinase and tyrosine phosphatase SHP-2

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JOURNAL OF BIOLOGICAL CHEMISTRY 2000年第12期275卷 8389-8396页

作者： Tang, H Zhao, ZZJ Landon, EJ Inagami, T Vanderbilt Univ Sch Med Dept Biochem Nashville TN 37232 USA Vanderbilt Univ Sch Med Dept Pharmacol Nashville TN 37232 USA Vanderbilt Univ Sch Med Div Hematol Nashville TN 37232 USA

Calcium-sensitive tyrosine kinase Pyk2 has been implicated in the regulation of ion channels, cellular adhesion, and mitogenic and hypertrophic reactions. In this study, we have investigated the regulation of Pyk2 by angiotensin II (Ang II) in pulmonary vein endothelial cells. We found that the Ang II-induced tyrosine phosphorylation of Pyk2, which requires the activity of Src family kinase, was specifically regulated by the Src family kinase member, Yes kinase, Moreover, we identified for the first time the constitutive association of Pyk2 with an Src homology 2 (SH2) domain-containing tyrosine phosphatase SHP-2. SHP-2 interacts with Pyk2 through a region other than its SH2 domains. Pyk2 can be dephosphorylated in vitro in SHP-2 immunoprecipitates and in intact cells expressing an NH, terminus-truncated form of SHP-2, which lacks the two SH2 domains but has an enhanced phosphatase activity. Ang II activates the endogenous SHP-2, Finally, the SHP-2-mediated dephosphorylation of Pyk2 correlates with the negative effect of SHP-2 on the Ang II-induced activation of extracellular signal-regulated kinase and c-Jun NH2-terminal kinase. Thus, the balance of Pyk2 tyrosine phosphorylation in response to Ang II is controlled by Yes kinase and by a tyrosine phosphatase SHP-2 in endothelial cells.

关键词：血管紧张素ⅱ/代谢内皮血管/细胞学内皮血管/生理学黏着斑激酶2 细胞内信号肽和蛋白质类 JNK丝裂原活化蛋白激酶类丝裂原激活蛋白激酶类/代谢磷酰化蛋白质结合蛋白质酪氨酸磷酸酶非受体1型蛋白质酪氨酸磷酸酶非受体11型蛋白酪氨酸磷酸酶非受体6型蛋白质酪氨酸磷酸酶类/代谢蛋白酪氨酸激酶类/代谢原癌基因蛋白质类/代谢原癌基因蛋白质c-fyn 原癌基因蛋白质c-yes 肺静脉/细胞学受体血管紧张素 1型受体血管紧张素 2型受体血管紧张素/代谢含SH2域蛋白质酪氨酸磷酸酶类信号传导酪氨酸/代谢 src族激酶类/代谢动物大鼠

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Angiotensin-II subtype 2 receptor agonist (CGP-42112) inhibits catecholamine biosynthesis in cultured porcine adrenal medullary chromaffin cells

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BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS 2000年第2期272卷 544-550页

作者： Takekoshi, K Ishii, K Isobe, K Nanmoku, T Kawakami, Y Nakai, T Univ Tsukuba Inst Clin Med Dept Clin Pathol Tsukuba Ibaraki 3058575 Japan

Angiotensin II subtype 2 receptor (AT(2)-R) is abundantly expressed in adrenal medullary chromaffin cells. However, the physiological roles of AT(2)-R in chromaffin cells remain to be clarified. Therefore, we investigated the effects of CGP42112 (AT(2)-R agonist) on catecholamine biosynthesis in cultured porcine adrenal medullary cells. We initially confirmed AT(2)-R was predominantly expressed in porcine adrenal medullary cells by [I-125]-Ang II binding studies. CGP42112 (greater than or equal to 1 nM) significantly inhibited cGMP production from the basal value. Tyrosine hydroxylase (TH) is a rate-limiting enzyme in the biosynthesis of catecholamine, and its activity is regulated by both TH-enzyme activity and TH-synthesis. CGP42112 (greater than or equal to 1 nM) significantly inhibited TH-enzyme activity from the basal value. These inhibitory effects of CGP42112 on TH-enzyme activity and-cGMP production were abolished by PD123319 (AT(2)-R antagonist) while CV-11974 (AT(1)-R antagonist) was ineffective. We also tested whether decrease of cGMP is involved in the inhibitory effect of CGP42112 on TH-enzyme activity. Pretreatment of 8-Br-cGMP (membrane-permeable cGMP analogue) prevented the inhibitory effect of CGP 42112 on TH-enzyme activity. Similar to that of TH-enzyme activity, CGP42112 (greater than or equal to 1 nM) significantly reduced TH-mRNA and TH-protein level from the basal value, and these inhibitory effects were abolished by PD123319 but not CV-11974. These findings demonstrate that CGP 42112 reduces both TH-enzyme activity and TH-synthesis and that these inhibitory effects could be mediated by decrease of cGMP production. (C) 2000 Academic Press.

关键词： 8-溴环腺苷一磷酸/药理学肾上腺髓质/细胞学肾上腺髓质/药物作用肾上腺髓质/酶学肾上腺髓质/代谢血管紧张素Ⅱ/拮抗剂和抑制剂血管紧张素ⅱ/代谢血管紧张素Ⅱ/药理学苯咪唑类/代谢苯咪唑类/药理学结合竞争性儿茶酚胺类/生物合成细胞培养的嗜铬细胞/细胞学嗜铬细胞/药物作用嗜铬细胞/酶学嗜铬细胞/代谢环GMP/类似物和衍生物环GMP/代谢环GMP/药理学剂量效应关系药物酶激活/药物作用酶诱导/药物作用咪唑类/代谢咪唑类/药理学寡肽类/拮抗剂和抑制剂寡肽类/代谢寡肽类/药理学吡啶类/代谢吡啶类/药理学 RNA 信使/遗传学 RNA 信使/代谢受体血管紧张素 1型受体血管紧张素 2型受体血管紧张素/激动剂受体血管紧张素/代谢猪四唑类/代谢四唑类/药理学酪氨酸单氧化酶/遗传学酪氨酸单氧化酶/代谢动物

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