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Suppression of angiotensin ⅱ stimulated responses in aortic vascular smooth muscle cells of experimental cirrhotic rats

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Cell Research 1999年第2期9卷 155-161页

作者： ZHANG RU GUO LIANG WANG PI LI ZHANG YING XIONG WEN BO ZHANG XING PENG WANG DE LING YIN QING JING (Shanghai Institute of Cell Biology, Chinese Academy of Sciences, 320 Yue Yang Road, Shanghai 200031, China )(Department of Gastroenterology, Shanghai F 2Department of Gastroenterology Shanghai First People s Hospital Shanghai Medical University 80 Wu Jin Road Shanghai 200080 China 2Department of Gastroenterology Shanghai First People s Hospital Shanghai Medical University 80 Wu Jin Road Shanghai 200080 China 2Department of Gastroenterology Shanghai First People s Hospital Shanghai Medical University 80 Wu Jin Road Shanghai 200080 China 1Shanghai Institute of Cell Biology Chinese Academy of Sciences 320 Yueyang Road Shanghai 200031 China 1Shanghai Institute of Cell Biology Chinese Academy of Sciences 320 Yueyang Road Shanghai 200031 China 2Department of Gastroenterology Shanghai First People s Hospital Shanghai Medical University 80 Wu Jin Road Shanghai 200080 China 1Shanghai Institute of Cell Biology Chinese Academy of Sciences 320 Yueyang Road Shanghai 200031 China 1Shanghai Institute of Cell Biology Chinese Academy of Sciences 320 Yueyang Road Shanghai 200031 China

Functional responses to angiotensin ⅱ (AT-Ⅱ) were determined in aortic vascular smooth muscle cells (VSMCs) from experimental cirrhotic rats. Our data showed that AT-Ⅱ-stimulated extracellular acidification rate (ECAR), which was measured by Cytosensor microphysiometry, was significantly reduced in the aortic VSMCs from the cirrhotic rats as compared to those from the control animals. The ability of AT-Ⅱ to promote formation of inositol phosphates, the second messenger produced by the activation of Gq-coupled receptors, was also considerably suppressed in the cirrhotic VSMCs. Furthermore, the maximal p42/44 MAPK phosphorylation stimulated by AT-Ⅱ was significantly reduced in the cirrhotic VSMCs in contrast to that in the normal VSMCs. Taken together, our data clearly demonstrated that the functional responses to AT-Ⅱ was severely suppressed in aortic VSMCs in cirrhosis, indicating the impairment of general Gq-coupled receptor signaling and subsequent biological function in the cirrhotic VSMCs.

关键词： angiotensin ⅱ aortic vascular smooth muscle cells, cirrhosis receptor responses

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Evodiamine Inhibits angiotensin ⅱ-Induced Rat Cardiomyocyte Hypertrophy

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Chinese Journal of Integrative Medicine 2018年第5期24卷 359-365页

作者： HE Na GONG Qi-hai ZHANG Feng ZHANG Jing-yi LIN Shu-xian HOU Hua-hua WU Qin SUN An-sheng Key Laboratory of Basic Pharmacology of Guizhou Departmentof Pharmacology Zunyi Medical College Zunyi GuizhouProvince (563099) China

Objective: To investigate the effects of evodiamine(Evo), a component of Evodiaminedia rutaecarpa(Juss.) Benth, on cardiomyocyte hypertrophy induced by angiotensin ⅱ(Ang Ⅱ) and further explore the potential mechanisms. Methods: Cardiomyocytes from neonatal Sprague Dawley rats were isolated and characterized, and then the cadiomyocyte cultures were randomly divided into control, model(Ang Ⅱ 0.1 μmol/L), and Evo(0.03, 0.3, 3 μmol/L) groups. The cardiomyocyte surface area, protein level, intracellular free calcium([Ca]i) concentration, activity of nitric oxide synthase(NOS) and content of nitric oxide(NO) were measured, respectively. The m RNA expressions of atrial natriuretic factor(ANF), calcineurin(CaN), extracellular signal-regulated kinase-2(ERK-2), and endothelial nitric oxide synthase(e NOS) of cardiomyocytes were analyzed by real-time reverse transcriptionpolymerase chain reaction. The protein expressions of calcineurin catalytic subunit(CnA) and mitogen-activated protein kinase phosphatase-1(MKP-1) were detected by Western blot analysis. Results: Compared with the control group, Ang Ⅱ induced cardiomyocytes hypertrophy, as evidenced by increased cardiomyocyte surface area, protein content, and ANF m RNA expression; increased intracellular free calcium([Ca]i) concentration and expressions of CaN m RNA, CnA protein, and ERK-2 m RNA, but decreased MKP-1 protein expression(P<0.05 or P<0.01). Compared with Ang Ⅱ, Evo(0.3, 3 μmol/L) significantly attenuated Ang Ⅱ-induced cardiomyocyte hypertrophy, decreased the [Ca]i concentration and expressions of CaN m RNA, CnA protein, and ERK-2 m RNA, but increased MKP-1 protein expression(P<0.05 or P<0.01). Most interestingly, Evo increased the NOS activity and NO production, and upregulated the e NOS m RNA expression(P<0.05). Conclusion: Evo significantly attenuated Ang Ⅱ-induced cardiomyocyte hypertrophy, and this effect was partly due to promotion of NO production, reduction of [Ca]i concentration, and inhibition of CaN and

关键词： evodiamine cardiomyocyte hypertrophy angiotensin ⅱ calcineurin extracellular signal regulated kinase-2 nitric oxide

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Rapamycin Treatment Attenuates angiotensin ⅱ-induced Abdominal Aortic Aneurysm Formation via VSMC Phenotypic Modulation and Down-regulation of ERK1/2 Activity

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Journal of Huazhong University of Science and Technology(Medical Sciences) 2018年第1期38卷 93-100页

作者： Fei-fei LI Xiao-ke SHANG Xin-ling DU Shu CHEN Department of Cardiovascular Surgery Union Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan 430022 China

The aim of the present study is to address the effect of rapamycin on abdominal aortic aneurysm（AAA） and the potential mechanisms. A clinically relevant AAA model was induced in apolipoprotein E-deficient（ApoE-/-） mice, in which miniosmotic pump was implanted subcutaneously to deliver angiotensin ⅱ（Ang Ⅱ） for 14 days. Male ApoE-/-mice were randomly divided into 3 groups： saline infusion, Ang Ⅱ infusion, and Ang Ⅱ infusion plus intraperitoneal injection of rapamycin. The diameter of the supra-renal abdominal aorta was measured by ultrasonography at the end of the infusion. Then aortic tissue was excised and examined by Western blotting and histoimmunochemistry. Ang Ⅱ with or without rapamycin treatment was applied to the cultured vascular smooth muscle cells（VSMCs） in vitro. The results revealed that rapamycin treatment significantly attenuated the incidence of Ang Ⅱinduced-AAA in ApoE-/-mice. Histologic analysis showed that rapamycin treatment decreased disarray of elastin fibers and VSMCs hyperplasia in the medial layer. Immunochemistry staining and Western blotting documented the increased phospho-ERKl/2 and ERK1/2 expression in aortic walls in Ang Ⅱ induced-AAA,as well as in human lesions. Whereas in the rapamycintreated group, decreased phospho-ERK1/2 expression level was detected. Moreover, rapamycin reversed Ang Ⅱ-induced VSMCs phenotypic change both in vivo and in vitro. Based on those results, we confirmed that rapamycin therapy suppressed Ang Ⅱ-induced AAA formation in mice, partially via VSMCs phenotypic modulation and down-regulation of ERK1/2 activity.

关键词： rapamycin abdominal aortic aneurysm angiotensin ⅱ extracellular signal-regulated kinase vascular smooth muscle cells phenotypic modulation

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angiotensin ⅱ-derived reactive oxygen species underpinning the processing of the cardiovascular reflexes in the medulla oblongata

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Neuroscience Bulletin 2011年第4期27卷 269-274页

作者： Valdir A.Braga Eduardo Colombari Mariana G.Jovita 坎皮纳联邦大学制药技术实验室圣保罗州立大学生理学与病理学系

The brainstem is a major site in the central nervous system involved in the processing of the cardiovascular reflexes such as the baroreflex and the peripheral chemoreflex. The nucleus tractus solitarius and the rostral ventrolateral medulla are 2 important brainstem nuclei, and they play pivotal roles in autonomic cardiovascular regulation. angiotensin II is one of the neurotransmitters involved in the processing of the known that one of the mechanisms by which angiotensin II exerts cardiovascular reflexes within the brainstem. It is well- its effect is via the activation of pathways that generate reactive oxygen species （ROS）. In the central nervous system, ROS are reported to be involved in several pathological dis- eases such as hypertension, heart failure and sleep apnea. However, little is known about the role of ROS in the processing of the cardiovascular reflexes within the brainstem. The present review mainly discussed some recent findings documenting a role for ROS in the processing of the baroreflex and the peripheral chemoreflex in the brainstem.

关键词： angiotensin ⅱ superoxide, rostral ventrolateral medulla nucleus tractus solitarius baroreflex peripheralchemoreflex

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Inhibitory effect of antisense oligodeoxynucleotide to p44/p42 MAPK on angiotensin ⅱ-induced hypertrophic response in cultured neonatal rat cardiac myocyte

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Acta Pharmacologica Sinica 2004年第1期 43-48页

作者： Shi-qin ZHANG, Bo DING, Zhao-gui GUO, Yun-xia LILaboratory of Molecular Pharmacology, Xiang Ya School of Medicine, Central South University, Changsha,, 410078,China

AIM: To explore the inhibitory effect of antisense oligonucleotide (ODN) to mitogen activated protein kinase (MAPK) on cardiomyocyte hypertrophy induced by angiotensin ⅱ (Ang Ⅱ). METHODS: A 17-mer phosphorothioate protected antisense ODN directed against the initiation of translation sites of the p42 and p44 MAPK isoforms by liposomal transfection was applied to inhibit the translation of p44/p42 MAPK mRNA. The sense and random ODNs to p44/p42MAPK were used as sequence controls. Neonatal cardiac myocytes were exposed to Ang Ⅱ (10 nmol/L) for 5 min and then harvested in lysis buffer for the measurement of the activity and the phosphorylated protein content of p44/p42MAPK that were tested by P-81 phosphocellulose filter paper method and Western blotting, respectively. The

关键词： mitogen-activated protein kinases antisense oligodeoxynucleotides angiotensin ⅱ hypertrophy myocardium

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Losartan inhibited expression of matrix metalloproteinases in rat atherosclerotic lesions and angiotensin ⅱ-stimulated macrophages

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Acta Pharmacologica Sinica 2004年第11期 42-48页

作者： Chun LIANG, Zong-gui WU, Jian DING, Jian-fei JIANG, Gao-zhong HUANG, Rong-zeng DU, Jun-bo GEDepartment of Cardiology, Changzheng Hospital, Second Military Medical University, Shanghai 200003, China Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai 201203, China Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, Shanghai 200032, China

AIM: To explore whether the angiotensin ⅱ (Ang Ⅱ) receptor 1 (AT1) antagonist, losartan could reduce activity and expression of matrix metalloproteinases (MMPs) in rat atherosclerotic plaques. METHODS: Male Wistar-Kyoto rats were ip injected a single dose of vitamin D3 600 kU·kg-1·month-1 and fed an atherogenic diet for 4 months to induce experimental atheroma. Then either placebo or losartan 50 mg·kg-1·d-1 was administered in rats for another 2 months. In vitro, the effect of losartan 0.1-10μmol/L on the expression of MMP-2 and MMP-9 was investigated in Ang II-stimulated rat peritoneal macrophages. The expression and activity of MMP-2 and MMP-9 were monitored by Western blot, RT-PCR, and SDS-PAGE zymography analysis. RESULTS: High levels of MMP-2 and MMP-9 were expressed in rat atherosclerotic lesions. Losartan significantly reduced the activity and expression of MMP-2 and MMP-9 compared with the placebo group (MMP-2, 5861±539 vs 8991±965, P<0.05; MMP-9, 10527±1002 vs 14623±2462, P<0.01). In

关键词： losartan metalloproteinases angiotensin ⅱ atherosclerosis peritoneal macrophages reverse tran-scriptase polymerase chain reaction Western blotting

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Effect of angiotensin ⅱ on Cord Blood CD^(34+) Cells Expansion in vitro

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Journal of Huazhong University of Science and Technology(Medical Sciences) 2005年第1期25卷 26-28页

作者：彭程邹萍马艳萍胡中波 Department of Hematology Union Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan 430022 China

In order to investigate the influence of angiotensin ⅱ on hematopoietic system, CD34 + cells in cord blood were purified, and the effects of angiotensin ⅱ in combination with various cytokines on their growth and differentiation were studied by cell culture in vitro. It was found that angiotensin ⅱ in suspending medium could stimulate both BFU-E and CFU-GM expansion. The number of BFU-E and CFU-GM was increased with the increases of angiotensin ⅱ concentrations during a certain range. In addition, the expansion fold of CFU-GM was increased from 2.3±0.8 times to 7.8±2.3 times when angiotensin ⅱ was added in the presence of SCF+G-CSF+GM-CSF+IL-3 cytokines mixture. Similarly, the expansion fold of BFU-E was increased from 3.1±1.8 times to 9 2±2.3 times with angiotensin ⅱ in the presence of SCF+EPO+TPO+IL-3. In the semi-solid medium, angiotensin ⅱ could stimulate CFU-GM expansion but had no effect on the growth of BFU-E. In conclusion, angiotensin ⅱ had some stimulating effects on cord blood hematopoietic progenitors expansion in vitro in the presence of other cytokines.

关键词： angiotensin ⅱ cord blood hematopoietic stem/progenitor cell ex vivo expansion

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Effects of Cyclosporine A on angiotensin ⅱ-induced Cardiomyocyte Hypertrophy in Neonatal Rats

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Journal of Huazhong University of Science and Technology(Medical Sciences) 2005年第5期25卷 558-560页

作者：韩召敏杨运海张凯伦向继洲 Department of Pharmacy Union Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan 430022 China Department of Cardiovascular Surgery Union Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan 430022 China Department of Pharmacology School of Basic Medical Sciences Tongji Medical College Huazhong University ofScience and Technology Wuhan 430022 China

Summary： The effects of cyclosporine A （CsA） on Angiontensin Ⅱ （Ang Ⅱ ）-induced protein contents, c los protein levels and cytosolic Ca^2＋ level （[Ca^2＋]i） in cultured eardiomyocytes of neonatal rats were observed. Total protein contents were determined by Bradford method. The expression of c-fos protein was detected by Western blot. （[Ca^2＋]i） labeled with fluorescent probe Fluo-3/AM was measured under a laser scanning confoeal microscope. The results revealed that as compared with control, the total protein contents were increased in cardiomyocytes treated with Ang Ⅱ （10-1 mol/ L）, which could be inhibited by CsA in a dose-dependent manner. It was found that Ang Ⅱ could increase the c-los protein expression, which could be inhibited by CsA in a dose-dependent manner. Ang Ⅱ induced the [Ca^2＋]i elevation in cardiomyocytes. CsA did not influence the resting intracellular Ca^2＋ , but inhibited significantly the Ang Ⅱ-induced [Ca^2＋]i elevation. It was concluded that CsA can suppress the Ang Ⅱ-induced c-fos protein expression and [Ca^2＋]i elevation in single cardiomyocyte, which might play a role in the prevention of Ang Ⅱ-induced cardiomyocyte hypertrophy by CsA.

关键词： cardiomyocyte hypertrophy angiotensin ⅱ cyclosporine A c-fos Ca2+

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Inhibition of angiotensin ⅱ and blockade of endothelin receptors reduce arterial calcification in rats

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Journal of Geriatric Cardiology 2004年第2期1卷 108-113页

作者： Juxiang LI~1 Shengying WU~1 Chunshui PAN~2 Yongfen QI~2 Bin GENG~1 Xiuhna LIU~~(1,2) Chaoshu TANG~1 1 Department of Physiology and Pathophysiology,Peking University Health Science Center,Beijing 100083,China 2 Insitiute of Cardiovascular Research,Peking University First Hospital,Beijing 100034,China Department of Physiology and Pathophysiology Peking University Health Science Center Beijing 100083 China Insitiute of Cardiovascular Research Peking University First Hospital Beijing 100034 China Department of Physiology and Pathophysiology Peking University Health Science Center Beijing 100083 China Insitiute of Cardiovascular Research Peking University First Hospital Beijing 100034 China

Objective To examine whether the two vascular paracrine/autocrine factors,angiotensin ⅱ(Ang Ⅱ)and endothelin,participate in the pathogenesis of arterial *** Nicotine and vitamin D_3 treated rats were *** calcification was confirmed by using Von Kossa staining,measurement of calcium content, ^(45)Ca^(2+)uptake assay and alkaline phosphatase(ALP)*** plasma and vascular Ang Ⅱ and endothelin levels were measured by using *** and endothehn mRNA levels were determined by RT- *** The arterial calcium content,^(45)Ca^(2+)uptake and ALP activity were increased in calcification groups compared with control(Pangiotensin receptor antagonist losartan,the endothelin receptor antagonist bosentan,and the angiotensin-converting enzyme inhibitor captopril reduced significantly the arterial calcium content,^(45)Ca^(2+)uptake and ALP *** addition,the plasma and aortic Ang Ⅱ and endothelin contents,and vascular angiotensinngen and endothelin mRNA expression were significantly up-regulated(Pangiotensin system and endothelin pathway are involved in vascular calcification,and that activation of these systems could potentiate pathogenesis of arterial calcification.(J Geriatr Cardiol 2004;1(2):108-113.)

关键词： aorta angiotensin ⅱ endothelin-1 calcification

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Effect of irbesartan on angiotensin ⅱ-induced hypertrophy of human proximal tubular cells

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Chinese Medical Journal 2004年第4期117卷 547-551页

作者：刘必成孙静陈琪罗冬冬马坤岭阮雄中 Institute of Nephrology Department of Pathophysiology Centre for Nephrology

Background Intrarenal activation of the renin angiotensin system (RAS) plays an important role in mediating renal fibrosis. Both angiotensin converting enzyme inhibitors (ACEIs) and angiotensin ⅱ (AngⅡ) receptor antagonists have been shown to exert a protective role against diabetic and non-diabetic nephropathy. However, the exact mechanism of how blocking local RAS prevents renal fibrosis is unclear. The present study was to investigate the influence of a new AngⅡ receptor antagonist, irbesartan (Irb), on AngⅡ-induced hypertrophy in human proximal tubular cell line (HK-2). Methods The cell line, HK-2, was grown in Dulbeccos’s Modified Eagle’s Medium containing 10% heat-inactivated fetal calf serum. After rested in serum-free medium for 24 hours, the effects of Irb on AngⅡ (10 -7 mol/L)-induced [ 3H]-leucine incorporation, total protein content (measured by the Coomassie brilliant blue G250 method), and change in cell size (determined by scanning electron microscopy) were observed. The influence of Irb on the cell cycle was analyzed by fluorescence activated cell sorter (FACS) flow cytometry. Results AngⅡ induced cell hypertrophy in a time and dose dependent manner. Stimulation of cells with AngⅡ for 48 hours resulted in a increase in [ 3H]-leucine incorporation [0 hour: (5584±1016) cpm/10 5cells vs 48 hours: (10741±802) cpm/10 5cells, P<0.05], which was significantly attenuated by treatment with Irb. AngⅡ significantly increased the total protein content in HK-2 cells [control: (0.169±0.011) mg/10 5cells vs AngⅡ group: (0.202±0.010) mg/10 5 cells, P<0.05], which was also markedly inhibited by cotreatment with Irb (P<0.01). Scanning electron microscopy showed that AngⅡ induced an increase in average physical cell size, which was significantly inhibited by Irb [control: (11.92±1.62) μm; AngⅡ group: (20.63±3.83) μm; AngⅡ+Irb group: (13.59±3.15) μm; P<0.01 vs control, respectively]. Furthermore, flow cytometry revealed that AngⅡ arrested cells in

关键词： irbesartan angiotensin ⅱ hypertrophy epithelial cells

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