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南方医科大学学报 2003年第3期23卷 219-221页

作者：张艺军杨希山吴平生李旭张晓峰陈晓清余中逊广州军区广州总医院老年二科510010

目的:探讨血管紧张素Ⅱ(AngⅡ)及其1型受体(AT1a)拮抗剂洛沙坦(losartan),对肝星状细胞(HSCs)生长、增殖的影响。方法:(1)分离大鼠HSCS,培养及鉴定;(2)在不同浓度的AngⅡ或losartan作用下,观察HSCs生长情况分别绘制细胞生长曲线、采用MT... 详细信息

目的:探讨血管紧张素Ⅱ(AngⅡ)及其1型受体(AT1a)拮抗剂洛沙坦(losartan),对肝星状细胞(HSCs)生长、增殖的影响。方法:(1)分离大鼠HSCS,培养及鉴定;(2)在不同浓度的AngⅡ或losartan作用下,观察HSCs生长情况分别绘制细胞生长曲线、采用MTT法、3H-胸腺嘧啶核苷掺入释放法检测AngⅡ或losartan对HSCs生长、增殖的影响。结果:AngⅡ刺激组在浓度高于10 E -9mol/L时,与对照组相比HSCs数量明显增多,DNA含量显著增加(P<0.05) ;losartan在浓度高于10 E-8mol/L时,HSCs数量明显减少,DNA含量显著降低(P<0.05);(losartan+AngⅡ)组HSCs数量与对照组相比无显著性差异(P>0.05)。结论:AngⅡ可以促使HSCs迅速增殖,其拮抗剂losartan明显抑制HSCs的生长、增殖。

关键词：肝硬化/病理学洛沙坦/药理学四唑类/药理学细胞分裂/药物作用星形细胞/药物作用血管紧张素ⅱ/药理学咪唑类/药理学大鼠动物

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心血管疾病发病机制研究:细胞外信号调节激酶在血管紧张素Ⅱ引起血管平滑肌细胞增殖反应中的调节作用

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中国临床康复 2004年第30期8卷 6614-6615页

作者：张严高秦永文吴弘文军慧李闻捷解放军南京军区杭州疗养院浙江省杭州市310007 解放军第二军医大学长海医院心内科上海市200433 解放军第二军医大学长海医院中心实验室上海市200433

目的:研究细胞外信号调节激酶(extracellularsignal-regulatedkinase,ERKs)信号途径在血管紧张素Ⅱ(angiotensinⅡ,AngⅡ)介导的大鼠血管平滑肌细胞(vascularsmoothmusclecell,VSMC)促增殖等反应中的作用及其可能的调控机制。方法:选用6周龄230g清洁级SD大鼠2只:本实验在长海医院中心实验室完成。实验依随机数字表分为正常对照组、AngⅡ诱导组、PD098059预处理组、U0126预处理组。每组均为3孔(n=3)。实验以通过3H-胸苷(3H-TdR)掺入率与3H-亮氨酸掺入率分别反映VSMC的DNA代谢与蛋白质合成代谢速率;并通过给予MAPK激酶特异性抑制剂PD098059及ERKs抑制剂UO126预处理,观察它们对细胞蛋白合成和DNA代谢及细胞增殖的影响。结果:①AngⅡ(1×10-7mmol/L)处理30minVSMC3H-胸苷掺入率和3H-亮氨酸掺入率均明显增高(增加207.2%,P<0.01);②AngⅡ增高3H-胸苷掺入的作用可明显被PD098059所抑制(增高抑制率52.3%,P<0.01)和完全被UO126所抑制(增高抑制率91.7%,P<0.01);③AngⅡ增高3H-亮氨酸掺入的作用可部分被PD098059所抑制(增加抑制率29.3%,P<0.05)和明显被UO126所抑制(增加抑制率64.6%,P<0.01)。结论:ERKs激活在血管紧张素Ⅱ导致VSMC增殖反应中具有重要作用,并可通过ERKs信号途径的特异性抑制剂的抑制效应,影响血管平?

关键词：肌平滑血管/细胞学血管紧张素ⅱ/药理学信号传导蛋白激酶/代谢

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Phosphorylation-mediated activation and translocation of the cyclic AMP-specific phosphodiesterase PDE4D3 by cyclic AMP-dependent protein kinase and mitogen-activated protein kinases - A potential mechanism allowing for the coordinated regulation of PDE4D activity and targeting

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JOURNAL OF BIOLOGICAL CHEMISTRY 1999年第15期274卷 10557-10565页

作者： Liu, HG Maurice, DH Queens Univ Pharmaceut Mfg Assoc Canada Hlth Res FdnMed Res Council Canada Dept Pathol Kingston ON K7L 3N6 Canada Queens Univ Dept Pharmacol & Toxicol Kingston ON K7L 3N6 Canada

In this study, we describe a novel mechanism by which a protein kinase C (PKC)-mediated activation of the Raf-extracellular signal-regulated kinase kinase (MEK)-extracellular signal-regulated kinase (ERK) cascade regulates the activity and membrane targeting of members of the cyclic AMP-specific phosphodiesterase D family (PDE4D), Using a combination of pharmacological and biochemical approaches, we show that increases in intracellular cAMP cause a protein kinase A-mediated phosphorylation and activation of the two PDE4D variants expressed in vascular smooth muscle cells, namely PDE4D3 and PDE4D5. In addition, we show that stimulation of PKC via the associated activation of the Raf-MEK-ERK cascade results in the phosphorylation and activation of PDE4D3 in these cells. Furthermore, our studies demonstrate that simultaneous activation of both the protein kinase A and PKC-Raf-MEK-ERK pathways allows for a coordinated activation of PDE4D3 and for the translocation of the particulate PDE4D3 to the cytosolic fraction of these cells. These data are presented and discussed in the context of the activation of the Raf-MEK-ERK cascade acting to modulate the activation and subcellular targeting of PDE4D gene products mediated by cAMP.

关键词： 3' 5'-环AMP磷酸二酯酶类/代谢血管紧张素ⅱ/药理学钙-钙调素依赖性蛋白激酶类/代谢细胞培养的环AMP依赖性蛋白激酶类/代谢环核苷酸磷酸二酯酶类 4型酶激活酶抑制剂/药理学肌平滑血管/酶学磷酰化蛋白激酶C/代谢十四酰佛波乙酯/药理学动物大鼠

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Expression of phosphodiesterase 4D (PDE4D) is regulated by both the cyclic AMP-dependent protein kinase and mitogen-activated protein kinase signaling pathways -: A potential mechanism allowing for the coordinated regulation of PDE4D activity and expression in cells

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JOURNAL OF BIOLOGICAL CHEMISTRY 2000年第34期275卷 26615-26624页

作者： Liu, HG Palmer, D Jimmo, SL Tilley, DG Dunkerley, HA Pang, SC Maurice, DH Queens Univ Dept Pathol Kingston ON K7L 3N6 Canada Queens Univ Dept Pharmacol & Toxicol Kingston ON K7L 3N6 Canada Queens Univ Dept Anat & Cell Biol Kingston ON K7L 3N6 Canada

Multiple families of cyclic nucleotide phosphodiesterases (PDE) have been described, and the regulated expression of these genes in cells is complex. Although cAMP is known to control the expression of certain PDE in cells, presumably reflecting a system of feedback on cAMP signaling, relatively little is known about the influence of non-cAMP signaling systems on PDE expression. In this study, we describe a novel mechanism by which activators of the protein kinase C (PKC)-Raf-MEK-ERK cascade regulate phosphodiesterase 4D (PDE4D) expression in vascular smooth muscle cells (VSMC) and assess the functional consequences of this effect. Whereas a prolonged elevation of cAMP in VSMC resulted in a protein kinase A (PHA)-dependent induction of expression of two PDE4D variants (PDE4D1 and PDE4D2), simultaneous activation of both the cAMP/-PKA and PRC-Raf-MER-ERK signaling cascades blunted this cAMP-mediated increase in PDE4D expression. By using biochemical, molecular biological, and pharmacological approaches, we demonstrate that this PDE4D-selective effect of activators of the PKC-Raf-MEK-ERK cascade was mediated through a mechanism involving altered PDE4D mRNA stability and markedly attenuated the cAMP-mediated desensitization that results from prolonged activation of the cAMP signaling system in cells. The data are presented in the context of activators of the PKC-Raf-MEK-ERK cascade having both short and long term effects on PDE4D activity and expression in cells that may influence cAMP signaling.

关键词： 8-溴环腺苷一磷酸/药理学血管紧张素ⅱ/药理学细胞培养的环AMP/代谢环AMP依赖性蛋白激酶类/生理学放线菌酮/药理学更生霉素/药理学酶抑制剂/药理学福司柯林/药理学异喹啉类/药理学丝裂原激活蛋白激酶激酶类/代谢丝裂原激活蛋白激酶类/生理学肌平滑血管/药物作用肌平滑血管/酶学蛋白激酶C/代谢蛋白质合成抑制药/药理学原癌基因蛋白质c-raf/代谢 RNA 信使/代谢信号传导磺胺类十四酰佛波乙酯/药理学动物大鼠

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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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Activation of the AT₁ angiotensin receptor is dependent on adjacent apolar residues in the carboxyl terminus of the third cytoplasmic loop

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JOURNAL OF BIOLOGICAL CHEMISTRY 2000年第21期275卷 15782-15788页

作者： Zhang, M Zhao, X Chen, HC Catt, KJ Hunyady, L Semmelweis Univ Sch Med Dept Physiol H-1444 Budapest Hungary NICHD Endocrinol & Reprod Res Branch NIH Bethesda MD 20892 USA

The C-terminal region of the third intracellular loop of the AT(1) angiotensin receptor (AT(1)-R) is an important determinant of G protein coupling. The roles of individual residues in agonist-induced activation of G(q/11)-dependent phosphoinositide hydrolysis were determined by mutational analysis of the amino acids in this region. Functional studies on mutant receptors transiently expressed in COS-7 cells showed that alanine substitutions of the amino acids in positions 232-240 of the third loop had no major effect on signal generation. However, deletion mutations that removed Ile(238) or affected its position relative to transmembrane helix VI significantly impaired angiotensin II-induced inositol phosphate responses. Substitution of Ile(238) with an acidic residue abolished the ability of the receptor to mediate inositol phosphate production, whereas its replacement with basic or polar residues reduced the amplitude of inositol phosphate responses. Substitutions of Phe(239) with polar residues had relatively minor effects on inositol phosphate signal generation, but its replacement by aspartic acid reduced, and by positively charged residues (Lys, Arg) significantly increased, angiotensin II-induced inositol phosphate responses. The internalization kinetics of the Ile(238) and Phe239 mutant receptors were impaired in parallel with the reduction in their signaling responses. These findings have identified Ile238 and Phe239 as the critical residues in the C-terminal region of the third intracellular loop of the AT(1)-R for receptor activation. They also suggest that an apolar amino acid corresponding to Ile(238) of the AT(1)-R is a general requirement for activation of other G protein-coupled receptors by their agonist ligands.

关键词：血管紧张素ⅱ/药理学 COS细胞 GTP结合蛋白质类/代谢肌醇磷酸类/代谢动力学膜蛋白质类/化学膜蛋白质类/遗传学突变蛋白质结合受体血管紧张素 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/化学受体血管紧张素/遗传学信号传导/遗传学转染动物大鼠

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Cloning and characterization of ATRAP, a novel protein that interacts with the angiotensin II type 1 receptor

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JOURNAL OF BIOLOGICAL CHEMISTRY 1999年第24期274卷 17058-17062页

作者： Daviet, L Lehtonen, JYA Tamura, K Griese, DP Horiuchi, M Dzau, VJ Harvard Univ Brigham & Womens Hosp Dept Med Boston MA 02115 USA

The carboxyl-terminal cytoplasmic domain of the angiotensin II type 1 (AT(1)) receptor has recently been shown to interact with several classes of cytoplasmic proteins that regulate different aspects of AT(1) receptor physiology. Employing yeast two-hybrid screening of a mouse kidney cDNA library with the carboxyl-terminal cytoplasmic domain of the murine AT(1a) receptor as a bait, we have isolated a novel protein with a predicted molecular mass of 18 kDa, which we have named ATRAP (for AT(1) receptor-associated protein). ATRAP interacts specifically with the carboxyl-terminal domain of the AT(1a) receptor but not with those of ansotensin II type 2 (AT(2)), m(3) muscarinic acetylcholine, bradykinin B-2, endothelin B, and beta(2)-adrenergic receptors, The mRNA of ATRAP was abundantly expressed in kidney, heart, and testis but was poorly expressed in lung, liver, spleen, and brain. The ATRAP-AT(1a) receptor association was confirmed by affinity chromatography, by specific co-immunoprecipitation of the two proteins, and by fluorescence microscopy, showing co-localization of these proteins in intact cells. Overexpression of ATRAP in COS-7 cells caused a marked inhibition of AT(1a) receptor-mediated activation of phospholipase C without affecting m(3) receptor-mediated activation. In conclusion, we have isolated a novel protein that interacts specifically with the carboxyl-terminal cytoplasmic domain of the AT(1a) receptor and affects AT(1a) receptor signaling.

关键词： 1-肌氨酸-8-异亮氨酸血管紧张素Ⅱ/类似物和衍生物 1-肌氨酸-8-异亮氨酸血管紧张素Ⅱ/代谢衔接蛋白质类信号转导氨基酸序列血管紧张素ⅱ/药理学碱基序列载体蛋白质类/遗传学载体蛋白质类/代谢克隆分子 DNA 互补/遗传学剂量效应关系药物酶激活分子序列数据蛋白质结合受体血管紧张素 1型受体血管紧张素 2型受体血管紧张素/代谢重组蛋白质类/代谢酿酒酵母菌/遗传学组织分布 C型磷脂酶类/代谢动物小鼠

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Low-dose angiotensin II reduces urinary cyclic AMP excretion in spontaneously hypertensive, but not normotensive, rats: Independence from hypertension and renal hemodynamic effects of angiotensin

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JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS 1999年第1期291卷 115-123页

作者： Jackson, EK Herzer, WA Mi, ZC Vyas, SJ Kost, CK Univ Pittsburgh Med Ctr Sch Med Ctr Clin PharmacolDept Pharmacol Pittsburgh PA 15213 USA Univ Pittsburgh Med Ctr Sch Med Ctr Clin PharmacolDept Med Pittsburgh PA 15213 USA

The purpose of this study was to determine whether the greater inhibitory effect of angiotensin II (Ang II) on urinary cAMP excretion in spontaneously hypertensive rats (SHRs) compared with normotensive Wistar-Kyoto (WKY) rats is secondary to hypertension and/or renal hemodynamic changes induced by Ang II. SHRs and WKY rats were treated chronically from conception, 6 weeks of age, or 10 weeks of age (n = 8-10) with the angiotensin-converting enzyme inhibitor captopril (100 mg/kg/ day). A fourth group was not treated chronically with captopril (n = 7). At similar to 13 weeks of age, all rats were anesthetized, given a bolus of captopril (30 mg/kg), and received an intrarenal infusion of a low dose of Ang II (1 ng/min). SHRs compared with WKY rats were normotensive, mildly hypertensive, and moderately hypertensive when treated with captopril from conception, 6 weeks of age, and 10 weeks of age, respectively, whereas untreated SHRs were severely hypertensive. In SHRs, Ang II decreased urinary cAMP excretion (p <.001), and this effect was independent of duration of captopril pretreatment (p = .696). In WKY rats, Ang II did not affect urinary cAMP excretion. Low-dose Ang II caused small and similar changes in renal blood flow and glomerular filtration rate in SHRs versus WKY rats and did not affect urine volume in either strain. We conclude that the greater effect of Ang II on urinary cAMP excretion in SHRs is not due to hypertension or to the renal hemodynamic effects of Ang II, but most likely to a greater effect of Ang II on some compartment of renal adenylyl cyclase activity in SHRs.

关键词：血管紧张素Ⅱ/投药和剂量血管紧张素ⅱ/药理学血管紧张素转换酶抑制药/药理学卡托普利/药理学环AMP/尿高血压/代谢高血压/尿肾/药物作用肾/生理学大鼠近交SHR 大鼠近交WKY 动物女(雌)性男(雄)性大鼠

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Angiotensin II-Induced renal vasoconstriction in genetic hypertension

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JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS 1999年第1期291卷 329-334页

作者： Jackson, EK Herzer, WA Vyas, SJ Kost, CK Univ Pittsburgh Med Ctr Ctr Clin Pharmacol Dept Pharmacol Pittsburgh PA 15213 USA Univ Pittsburgh Med Ctr Ctr Clin Pharmacol Dept Med Pittsburgh PA 15213 USA

Previous studies demonstrate that renovascular responses to angiotensin II (Ang II) are enhanced in spontaneously hypertensive rats (SHRs);however, it is possible that this hyperresponsiveness is mediated by Ang II-induced release of substances from the adrenal gland. Previous studies also show that pertussis toxin normalizes renovascular responses to Ang II in SHRs;however, it is possible that this response is mediated by effects of pertussis toxin on endogenous Ang II levels and/or the sympathoadrenal axis. The purpose of this study was 2-fold: 1) to determine whether the renovascular response to Ang II in SHRs is enhanced even in adrenalectomized SHRs and 2) to determine whether pertussis toxin normalizes enhanced renovascular responses to Ang II when pertussis toxin-induced changes in the renin-angiotensin system and the sympathoadrenal axis are prevented. SHRs and Wistar Kyoto (WKY) rats were anesthetized and administered 20 ml/kg 0.9% saline, and an infusion of aldosterone and hydrocortisone was initiated. After bilateral adrenalectomy, left renal denervation, and pretreatment with captopril, animals received an intrarenal artery infusion of Ang II at 10 ng/kg/min for 5 min. Ang II-induced changes in renal vascular resistance were greater in SHRs compared with WKY rats (p = .010, n = 19/group). Pertussis toxin (10 mu g/kg i.v. 3 days before the experiment) attenuated Ang II-induced changes in renal vascular resistance in SHR (p<.05), but not in WKY rats (strain 3 treatment interaction: p = .046). These results suggest that the enhanced renovascular response to Ang II in SHRs is mediated by a G(i)-dependent pathway within the renal vasculature.

关键词：方差分析血管紧张素ⅱ/药理学血压/药物作用儿茶酚胺类/药理学药物相互作用高血压/遗传学高血压/病理生理学肾/药物作用肾/病理生理学百白咳毒素大鼠近交SHR 大鼠近交WKY 肾循环/药物作用血管阻力/药物作用血管收缩/药物作用毒力因子鲍特菌属/药理学动物大鼠

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Restriction of placental and fetal growth in sheep alters fetal blood pressure responses to angiotensin II and captopril

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JOURNAL OF PHYSIOLOGY-LONDON 1999年第3期515卷 897-904页

作者： Edwards, LJ Simonetta, G Owens, JA Robinson, JS McMillen, IC Univ Adelaide Dept Physiol Adelaide SA 5005 Australia Univ Adelaide Dept Obstet & Gynecol Adelaide SA 5005 Australia

1. We have measured arterial blood pressure between 115 and 145 days gestation in normally grown fetal sheep (control group;n = 16) and in fetal sheep in which growth was restricted by experimental restriction of placental growth and development (PR group;n = 13). There was no significant difference in the mean gestational arterial blood pressure between the PR (42.7 +/- 2.6 mmHg) and control groups (37.7 +/- 2.3 mmHg). Mean arterial blood pressure and arterial P-O2 were significantly correlated in control animals (r = 0.53, P < 0.05, n = 16), but not in the PR, group. 2. There were no changes in mean arterial blood pressure in either the PR or control groups in response to captopril (7.5 mu g captopril min(-1);PR group n = 7, control group n = 6) between 115 and 125 days gestation. After 135 days gestation, there was a significant decrease (P < 0.05) in the fetal arterial blood pressure in the PR group but not in the control group during the captopril infusion (15 mu g captopril min(-1);PR group n = 7, control group n = 6). 3. There was a significant effect (F = 14.75;P < 0.001) of increasing doses of angiotensin II on fetal diastolic blood pressure in the PR and control groups. The effects of angiotensin II n ere different (F = 8.67;P < 0.05) in the PR and control groups at both gestational age ranges. 4. These data indicate that arterial blood pressure may be maintained by different mechanisms in growth restricted fetuses and normally grown counterparts and suggests a role for the fetal renin-angiotensin system in the maintenance of blood pressure in growth restricted fetuses.

关键词：血管紧张素ⅱ/药理学血压/药物作用血压/生理学卡托普利/药理学心舒期胚胎和胎儿发育/生理学胎儿生长迟缓/病理生理学胎儿心脏/药物作用胎儿心脏/生理学胎儿心脏/病理生理学孕龄氧/血液胎盘/生理学绵羊心缩期动物女(雌)性妊娠

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