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中国医师杂志 2015年第7期17卷 1053-1055页

作者：孟秋云张福业逄小红陈燕赵廷利孙焕香李桂英张雪岩泰安市第四人民医院心内科山东省泰安271000 泰山医学院学报编辑部

目的探讨原发性高血压患者血浆内皮素-1（ET-1）水平及晨尿白蛋白/肌酐比值（UACR）与高血压及血压变异的关系.方法根据《2010年中国高血压防治指南》的血压标准,筛选出104例高血压病患者,按高血压分为1～3级,共分3个组实验组,另选择... 详细信息

目的探讨原发性高血压患者血浆内皮素-1（ET-1）水平及晨尿白蛋白/肌酐比值（UACR）与高血压及血压变异的关系.方法根据《2010年中国高血压防治指南》的血压标准,筛选出104例高血压病患者,按高血压分为1～3级,共分3个组实验组,另选择同期本院体检中心体检健康者45例为对照组,所有对象均进行无创性24 h动态血压监测,并检测血管内皮功能障碍的标志物：ET-1及UACR的水平.结果与正常对照组比较,高血压组ET-1、UACR的水平明显升高（P＜0.05,P ＜0.01）,且随着血压的增高而增高,与24h平均收缩压（24 h SBP）、24h平均舒张压（24 h DBP）、24h收缩压变异系数（24h SCV）、24 h舒张压变异系数（24 h DCV）呈正相关（P＜0.05,P＜0.01）.多元逐步回归分析表明：校正血糖、胆固醇、甘油三酯、体质量指数、高血压病程后,ET-1及UACR的水平仍与24 h SBP、24 h DBP、24 h SCV呈正相关（P＜0.01）;24h DCV与ET-1呈正相关（P＜0.05）、与UACR无相关（P＞0.05）.结论原发性高血压患者存在血管内皮功能障碍,血管内皮损伤不仅与血压水平有关,而且与血压变异相关;其损伤的程度不仅与血压升高的严重程度密切相关,而且与血压变异的严重程度密切相关,特别是收缩压变异.

关键词：内皮缩血管肽1/代谢白蛋白尿肌酸酐/代谢高血压血压

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川崎病患儿内皮素1和肌钙蛋白1水平动态变化的研究

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中国医师杂志 2011年第5期13卷 608-610页

作者：汤卫红管敏昌江雪娟沈新光林丹温州医学院附属台州医院路桥院区浙江省台州318050 恩泽妇产医院

目的探讨川崎病（kawasaki disease，KD）患儿急性期后内皮素1（ET-1）和心肌肌钙蛋白I（cTnI）变化的临床意义。方法本院60例川崎病患儿中合并冠状动脉病变者12例，未合并冠状动脉病变者48例，分别测定川崎病患儿及30例健康儿童血浆内... 详细信息

目的探讨川崎病（kawasaki disease，KD）患儿急性期后内皮素1（ET-1）和心肌肌钙蛋白I（cTnI）变化的临床意义。方法本院60例川崎病患儿中合并冠状动脉病变者12例，未合并冠状动脉病变者48例，分别测定川崎病患儿及30例健康儿童血浆内皮素1、血清肌钙蛋白I水平，分析病例组急性期和恢复期患儿血浆ET-1与血清cTnI变化，与健康儿童进行对照。结果合并冠状动脉病变（CAL）组急性期ET-1、cTnl分别为（90．19±3．43）ng／L,（1．35±0．14）μg／L，其恢复期ET-1、cTnl分别为（89．09±2．44）ng／L、（1．12±0．11）μg／L，两组比较差异均无统计学意义（P〉0．05）；无冠状动脉损伤（NCAL）组急性期ET-1、cTnI浓度值分别为（64.494±4．78）ng／L、（0．62±0．02）μg／L，恢复期ET-1、cTnI浓度值分别为（50．474±4．49）ng／L、（0．07±0．05）μg／L，两组比较差异均有统计学意义（P〈0．01）。川崎病患儿急性期和恢复期血浆ET-1与血清cTnI浓度呈正相关（r=0．93，0．96，P〈0．01）。结论川崎病合并冠状动脉病变患儿血浆内皮素1水平与血清肌钙蛋白I水平相关，可作为川崎病合并冠状动脉病变的早期风险监测指标。

关键词：黏膜皮肤淋巴结综合征/代谢内皮缩血管肽1/代谢肌钙蛋白I/代谢

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不同大小剪切力对血管内皮细胞IL-8及ET-1表达的影响

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中国医师杂志 2018年第5期20卷 667-671页

作者：范涛于晓东陈春玲新疆医科大学第一附属医院麻醉科乌鲁木齐830054

目的探讨不同大小剪切力对血管内皮细胞白介素-8(IL-8)及内皮素-1(ET-1)表达的影响。方法采用脐静脉内皮细胞株(ECV-304)作为研究细胞,使用自制的剪切力调控装置调节出5 dyne/cm^2和10 dyne/cm^2的剪切力,其中5 dyne/cm^2的剪切力作为... 详细信息

目的探讨不同大小剪切力对血管内皮细胞白介素-8(IL-8)及内皮素-1(ET-1)表达的影响。方法采用脐静脉内皮细胞株(ECV-304)作为研究细胞,使用自制的剪切力调控装置调节出5 dyne/cm^2和10 dyne/cm^2的剪切力,其中5 dyne/cm^2的剪切力作为低剪切力组,10 dyne/cm^2的剪切力作为高剪切力组,另选用未施加剪切力的ECV-304作为对照组。分析三组在五个时间点(30、60、120、300、420 min)的IL-8和ET-1水平,并采用Pearson相关分析方法分析IL-8和ET-1水平的相关性。结果三组的IL-8水平一直呈上升趋势。在30、60、120 min三个时间点,三组的IL-8水平整体比较差异无统计学意义(P>0.05)。在300、420 min两个时间点,低剪切力组的IL-8水平高于对照组和高剪切力组,高剪切力组的IL-8水平高于对照组(P<0.05)。对照组和低剪切力组的ET-1水平一直呈上升趋势,高剪切力组的JET-1水平在前120 min持续上升,但在此后开始持续下降。在30、60、120 min三个时间点,三组的ET-1水平整体比较差异具有统计学意义(P<0.05),高剪切力组在30、60、120 min三个时间点的ET-1水平均高于对照组,在30、60 min两个时间点的ET-1水平高于低剪切力组(P<0.05);低剪切力组在60、120 min两个时间点的ET-1水平高于对照组(P<0.05);在300、420 min两个时间点,三组的ET-1水平整体比较差异无统计学意义(P>0.05)。Pearson相关分析显示,IL-8与ET-1的表达存在正相关关系(r=0.384,P=0.031)。结论剪切力可对血管内皮细胞IL-8、ET-1的表达造成影响,其中5 dyne/cm^2的剪切力能够更高效地增加IL-8水平,10 dyne/cm^2的剪切力能够更明显地增加ET-1水平,但可能会对血管内皮细胞造成损伤。

关键词：粘度内皮,血管/代谢内皮细胞/代谢白细胞介素8/代谢内皮缩血管肽1/代谢

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大鼠肢体缺血/再灌注后NO/ET-1平衡与脑组织氧化损伤关系的研究

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陕西医学杂志 2006年第1期35卷 18-21页

作者：胡永奇张连元李宏杰彭军董淑云门秀丽杨全会华北煤炭医学院病理生理教研室唐山063000

目的:研究一氧化氮(NO)和内皮素-1(ET-1)在大鼠肢体缺血/再灌注(L I/R)后脑氧化损伤中的作用,探讨NO/ET-1平衡关系的变化对脑损伤的影响。方法:在大鼠L I/R损伤模型上,观察血浆NO,ET-1,MDA,XOD,SOD,LDH,CK及脑组织tNOS,iNOS,cNOS,NO,ET-... 详细信息

目的:研究一氧化氮(NO)和内皮素-1(ET-1)在大鼠肢体缺血/再灌注(L I/R)后脑氧化损伤中的作用,探讨NO/ET-1平衡关系的变化对脑损伤的影响。方法:在大鼠L I/R损伤模型上,观察血浆NO,ET-1,MDA,XOD,SOD,LDH,CK及脑组织tNOS,iNOS,cNOS,NO,ET-1,MDA,XOD,M PO,SOD,W/D的变化。结果:L I/R后血浆LDH,CK,MDA,XOD和脑组织MDA,XOD,M PO,W/D较对照组升高,自由基清除酶SOD活性下降,在再灌注4h脑组织损伤最为严重。再灌后,脑组织tNOS和iNOS活性升高,而cNOS活性降低,血浆及脑组织中NO,ET-1增加,NO/ET-1比值降低,在再灌注4h降低最为明显。结论:大鼠L I/R后脑损伤的发生可能与机体自由基产生增多,清除酶活性下降以及NO/ET-1失平衡有关。

关键词：再灌注损伤/血液再灌注损伤/病理学脑损伤/病理学一氧化氮/代谢内皮缩血管肽1/代谢四肢大鼠

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Prolonged infusions of estradiol dilate the ovine fetal pulmonary circulation

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PEDIATRIC RESEARCH 2000年第1期47卷 89-96页

作者： Parker, TA Kinsella, JP Galan, HL Le Cras, TD Richter, GT Markham, NE Abman, SH Univ Colorado Sch Med Dept Pediat Denver CO 80262 USA Univ Colorado Sch Med Pediat Heart Lung Ctr Denver CO 80262 USA Univ Colorado Sch Med Dept Obstet & Gynecol Denver CO 80262 USA

Factors mediating both the rapid and sustained fall in pulmonary vascular resistance (PVR) at birth are incompletely understood. Acute or prolonged estrogen treatment causes vasodilation of several vascular beds in adults. Although fetal estrogen levels rise in late gestation, their effects in the fetal pulmonary circulation have not been studied. To determine whether estrogens can cause pulmonary vasodilation in the fetus, we infused 17 beta-estradiol (E2) into the left pulmonary artery (LPA) of chronically catheterized fetal lambs, measured pulmonary artery pressure and LPA blood how, and calculated PVR. Brief E2 administration (1-, 10-, and 100-mu g doses) did not change baseline pulmonary hemodynamics and failed to enhance endothelium-dependent vasodilation as assessed by the dilator response to acetylcholine. However, prolonged E2 infusion (2-8 d) caused a 2.6-fold increase in pulmonary blood how (73 +/- 6 versus 188 +/- 44 mL/min, baseline versus E2 treatment, p < 0.05), and the response was sustained for at least several hours. Treatment with the nitric oxide synthase inhibitor nitro-L-arginine (L-NA) reversed the E2-induced fall in PVR (0.15 +/- 0.05 versus 0.51 +/- 0.15 mm Hg/mL/min;before versus after L-NA, p < 0.05). Endothelial nitric oxide synthase expression and endothelin-1 content were not different in E2-responders and controls, suggesting that altered expression of these mediators did not account for the increased flow. We conclude that prolonged E2 infusion causes an unusual pattern of vasodilation in the ovine fetal lung. On the basis of these observations of exogenous E2 treatment, we speculate that endogenous E2 enhances pulmonary vasodilation at birth.

关键词：内皮缩血管肽1/代谢雌二醇/投药和剂量雌二醇/药理学胎儿/血液供给一氧化氮合酶/拮抗剂和抑制剂一氧化氮合酶/代谢一氧化氮合酶Ⅲ型肺动脉/药物作用肺动脉/胚胎学肺动脉/生理学绵羊/胚胎学血管舒张/药物作用动物

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Endothelin receptor blockade inhibits molecular effectors of Kaposi's sarcoma cell invasion and tumor growth in vivo

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AMERICAN JOURNAL OF PATHOLOGY 2003年第2期163卷 753-762页

作者： Rosanò, L Spinella, F Di Castro, V Nicotra, MR Albini, A Natali, PG Bagnato, A Regina Elena Inst Canc Res Lab Mol Pathol & Ultrastruct I-00158 Rome Italy Regina Elena Inst Canc Res Dept Immunol I-00158 Rome Italy CNR Mol Biol & Pathol Inst Rome Italy Natl Inst Canc Res Ctr Adv Biotechnol Genoa Italy

Endothelin-1 (ET-1) and its receptors are overexpressed in human Kaposi's sarcoma lesions. Here we show that in human KS IMM cell line ET-1 increased secretion and activation of matrix-metalloproteinase-2 (MMP-2), -3, -7, -9 and -13, as well as of membrane-type 1-MMP (MT1-MMP). ET-1 and ET-3 also enhanced the expression of tissue inhibitor of MMP-2, essential for MT1-MMP-mediated MMP-2 activation. Combined addition of both ETB receptor (ETBR) and ETAR antagonists completely blocked the ET-1-induced MMP activity. By immunohistochemistry, we observed that ET-1 increased MMP-2 and MT1-MMP expression and their localization at the cell surface. Treatment with both antagonists resulted also in the suppression of ET-1-induced phosphorylation of focal adhesion proteins, FAK and paxillin, which are essentials for cell motility. ET-1 induced a dose-dependent enhancement in KS IMM cell migration and MMP-dependent invasiveness that were inhibited by ET-1 receptor antagonists. The small molecule, A-182086, an orally bioavailable ETA/BR antagonist, completely inhibited cell proliferation and tumor growth in KS IMM xenografts. These findings demonstrate that ET-1-driven autocrine loop is crucial for enhanced invasiveness of KS IMM cells and promote tumor growth in vivo. Such activities can be blocked by the ETA/BR antagonists, which may be effective anti-angiogenic and anti-tumor molecules for the treatment of Kaposi's sarcoma.

关键词：细胞分裂/生理学细胞运动/生理学细胞移植培养基条件性细胞支架蛋白质类/代谢内皮缩血管肽1/代谢内皮缩血管肽3/代谢酶激活黏着斑激酶1 黏着斑蛋白酪氨酸激酶类基质金属蛋白酶类/遗传学基质金属蛋白酶类/代谢小鼠裸桩蛋白磷蛋白类/代谢蛋白酪氨酸激酶类/代谢受体内皮素A 受体内皮素B 受体内皮缩血管肽/拮抗剂和抑制剂受体内皮缩血管肽/代谢肉瘤卡波西/代谢肉瘤卡波西/病理学金属蛋白酶2组织抑制剂/代谢肿瘤细胞培养的动物女(雌)性人类小鼠

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Down-regulation of endothelin-B receptor sites in cavernosal tissue of a rabbit model of partial bladder outlet obstruction: potential clinical relevance

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WORLD JOURNAL OF UROLOGY 1999年第5期17卷 290-295页

作者： Khan, MA Dashwood, MR Thompson, CS Auld, J Morgan, RJ Mikhailidis, DP Royal Free Hosp Royal Free & Univ Coll Med Sch Dept Urol London NW3 2QG England Royal Free & Univ Coll Med Sch Dept Mol Pathol & Clin Biochem London England Royal Free Hampstead NHS Trust London England UCL Royal Free & Univ Coll Med Sch Dept Immunocytochem London England

Erectile dysfunction (ED) is a common problem that significantly affects quality of life and psychological well-being. Benign prostatic hyperplasia (BPH) is the commonest known benign proliferative disorder. Recently there has been growing evidence to suggest that patients with high BPH symptom scores have an increased incidence of ED. Endothelin-1 (ET-1) is a potent vasoconstrictor peptide that is thought to play an important role as a modulator of erectile physiology and dysfunction. We investigated whether there were any changes in the penile histology and in the density and distribution of ET-1 and its receptor subtypes in the corpora cavernosa of a rabbit model of partial bladder outflow obstruction (BOO). BOO was induced in 12 adult New Zealand White rabbits;12 sham-operated rabbits acted as controls. Penises were excised after 3 and 6 weeks (n = 6 each for control and BOO). Low- and high-resolution autoradiography was performed using radioligands for ET-1, ET(A) and ET(B) receptors and the results were analysed densitometrically. Ultrastructural evaluation of the corpus cavernosum (CC) was also performed. ET-1, ET(A) and ET(B) receptor-binding sites were primarily localised to the smooth-muscle cells (SMC) of the CC and to the endothelium lining the cavernosal space. ET(B) receptor-binding sites were significantly decreased (P = 0.04) in the 6-week BOO cavernosal tissue. These receptor changes were accompanied by ultrastructural changes in the CC. ET-1 may play a role in the pathophysiology of ED associated with BPH. This may partly be due to enhanced vasoconstrictor actions and SMC proliferation secondary to a reduction in ET(B) receptors. Further work is needed to evaluate this possibility.

关键词：肌动蛋白类/分析抗原 CD31/分析放射自显影术血糖血尿素氮减量调节/生理学电解质/血液内皮缩血管肽1/分析内皮缩血管肽1/代谢碘放射性同位素/诊断应用显微镜检查电子显微镜检查电子扫描阴茎/化学阴茎/超微结构受体内皮素A 受体内皮素B 受体内皮缩血管肽/分析受体内皮缩血管肽/代谢膀胱/化学膀胱/病理生理学膀胱/超微结构膀胱颈梗阻/代谢动物男(雄)性兔

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Vascular dysfunction and heart failure: Epiphenomenon or etiologic agent?

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AMERICAN HEART JOURNAL 2002年第3期143卷 383-390页

作者： Fang, ZY Marwick, TH Univ Queensland Dept Med Brisbane Qld 4000 Australia

Endothelial function plays a key role in the local regulation of vascular tone. Alterations in endothelial function may result in impaired release of endothelium-derived relaxing factors or increased release of endothelium-derived contracting factors. Heart failure may impair endothelial function by means of reduced synthesis and release of nitric oxide (NO) or by increased degradation of NO and increased production of endothelin-1. Endothelial dysfunction may worsen heart function by means of peripheral effects, causing increased afterload and central effects such as myocardial ischemia and inducible nitric oxide synthase (iNOS)-induced detrimental effects. Evidence from clinical studies has suggested that there is a correlation between decreased endothelial function and increasing severity of congestive heart failure (CHF). Treatments that improve heart function may also improve endothelial dysfunction. The relationship between endothelial dysfunction and heart failure may be masked by the stage of endothelial dysfunction, the location of vessels being tested, and the state of endothelial-dependent vasodilatation response.

关键词：内皮缩血管肽1/代谢内皮血管/生理学心力衰竭/病因学心力衰竭/代谢心力衰竭/病理生理学一氧化氮/代谢一氧化氮/生理学一氧化氮合酶/代谢一氧化氮合酶/生理学一氧化氮合酶Ⅱ型一氧化氮合酶Ⅲ型肿瘤坏死因子α/生理学血管收缩血管舒张人类

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Late endosomal/lysosomal targeting and lack of recycling of the ligand-occupied endothelin B receptor

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MOLECULAR PHARMACOLOGY 2000年第6期57卷 1104-1113页

作者： Oksche, A Boese, G Horstmeyer, A Furkert, J Beyermann, M Bienert, M Rosenthal, W Forschungsinst Mol Pharmakol D-10315 Berlin Germany Free Univ Berlin Inst Pharmakol D-1000 Berlin Germany

A fusion protein consisting of the endothelin B (ETB) receptor and the enhanced green fluorescent protein (EGFP) in conjunction with Cyanin3- or fluorescein-conjugated endothelin 1 (Cy3-ET1, Fluo-ET1) was used to investigate the ligand-mediated internalization of the ETB receptor. The ETB receptor and the ETB/EGFP fusion protein displayed very similar pharmacological properties when expressed in Chinese hamster ovary cells. The integrity of the fusion protein was verified by low temperature PAGE analysis of the I-125-ET1-bound ETB receptor and the I-125-ET1-bound ETB/EGFP fusion protein. Fluorescence microscopy of Chinese hamster ovary cells expressing the ETB/EGFP fusion protein demonstrated strong signals at the plasma membrane. On addition of Cy3-ET1, internalization of ligand and receptor occurred within 5 min via a sucrose-sensitive (i.e., clathrin-mediated) pathway. On further incubation, ETB/EGFP and Cy3-ET1 fluorescences were found in the perinuclear region, colocalized with fluorescent low density lipoproteins, a marker of the late endosomal/lysosomal pathway, but not with fluorescent transferrin, a marker of the recycling pathway. No dissociation of Cy3-ET1 from the receptor was seen within 4 h. Using I-125-ET1 or Cy3-ET1, binding sites were again demonstrable at the cell surface within 2 h. The reappearance of binding sites was abolished by prior treatment of the cells with cycloheximide, an inhibitor of protein synthesis. The data demonstrate that the ligand-occupied ETB receptor is internalized;however, it does not recycle like most of the G protein-coupled receptors but is sorted to the late endosomal/lysosomal pathway in a manner similar to that of the family of protease-activated receptors.

关键词：氨基酸序列 CHO细胞仓鼠亚科减量调节内颗粒/生理学内皮缩血管肽1/代谢配体溶酶体/生理学显微镜检查荧光分子序列数据吞噬作用受体内皮素B 受体内皮缩血管肽/代谢动物

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CARDIOVASCULAR AND ORGAN RESPONSES AND ADAPTATION RESPONSES TO HYPOGRAVITY IN AN EXPERIMENTAL ANIMAL-MODEL

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ACTA ASTRONAUTICA 1995年第C期37卷 373-377页

作者： BIONDI, R CAPODICASA, E TASSI, C MEZZASOMA, L BENEDETTI, C VALIANI, M MARCONI, P ROSSI, R UNIV PERUGIA DEPT CLIN MED PATHOL & PHARMACOLGEN PATHOL & IMMUNOL SECTI-06100 PERUGIAITALY

The head-down suspension (i.e antiorthostatic hypokinesia) rat is used to simulate weightlessness. However, little is known about cardiovascular and organ adaptation responses which, over a long time, can become pathologically significant. The purpose of this study was therefore to evaluate regional changes in the hematology parameters, Endotheline-1 (ET-I) concentration and urinary excretion of N-acetyl-beta-D-glucosaminidase (EC 3.2.1.30) (NAG) in experimental antiorthostatic rat model. The indicate significant variations in the plasma ET-I level in time, in the superior and inferior cava vessel blood of animals maintained for 10 days in hypogravity with respect to controls. These changes do not seem to be due to hemoconcentration. The increase in urinary NAG was observed during the first 24h of experiment, indicating renal stress, probably due to adverse blood flow variations within the organ. We conclude that the plasma ET-I level changes could be responsible, overall for the blood flow variations in the kidney and renal stress could be the consequence of extended antiorthostatic hypokinesia. The ET-1 behaviour and urinary NAG excretion in rats exposed to antiorthostatic hypokinetic hydynamia offer possibilities for understanding if these changes might be reversible or when they become pathological. This could give some relevant information about the effects of prolonged hypogravity during the space voyage.

关键词：乙酰氨基葡糖苷酶/代谢乙酰氨基葡糖苷酶/尿适应生理学/生理学内皮缩血管肽1/血液内皮缩血管肽1/代谢内皮缩血管肽2/血液内皮缩血管肽2/代谢头低位后肢悬吊大鼠 Sprague-Dawley 肾循环腔静脉下腔静脉上失重模拟动物男(雄)性大鼠

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