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Nitric oxide synthase 3-dependent vascular remodeling and circulatory dysfunction in cirrhosis

AMERICAN JOURNAL OF PATHOLOGY 2003年第6期162卷 1985-1993页

作者： Fernández-Varo, G Ros, J Morales-Ruiz, M Cejudo-Martín, P Arroyo, V Solé, M Rivera, F Rodés, J Jiménez, W Univ Barcelona Hosp Clin Barcelona Inst Invest Biomed August Pi i Sunyer Hormonal Lab E-08036 Barcelona Spain Univ Barcelona Hosp Clin Barcelona Inst Invest Biomed August Pi i Sunyer Liver Unit E-08036 Barcelona Spain Univ Barcelona Hosp Clin Barcelona Inst Invest Biomed August Pi i Sunyer Dept Pathol E-08036 Barcelona Spain Inst Reina Sofia Invest Nefrol Barcelona Spain

Vascular remodeling is an active process that consists in important modifications in the vessel wall. Endothelium derived nitric oxide (NO) plays a major role in this phenomenon. We assessed wall thickness (WT), total wall area (TWA), lumen diameter, and total nuclei number/cross-section (TN) in cirrhotic rats with ascites;and in control rats. A second group of cirrhotic rats received the NO synthesis inhibitor, L-NAME, or vehicle daily for 11 weeks and systemic hemodynamics, arterial compliance, aortic NO synthase 3 (NOS3) protein expression, and vascular morphology were analyzed. Cirrhotic vessels showed a significant reduction in WT, TWA, and TN as compared to control vessels. Long-term inhibition of NOS activity in cirrhotic rats resulted in a significant increase in WT, TWA, and TN as compared to cirrhotic rats receiving vehicle. NOS3 protein abundance was higher in aortic vessels of nontreated cirrhotic animals than in controls. This difference was abolished by chronic treatment with L-NAME. NOS inhibition in cirrhotic rats resulted in higher arterial pressure and peripheral resistance and lower arterial compliance than cirrhotic rats receiving vehicle. Therefore, vascular remodeling in cirrhosis with ascites is a generalized process with significant functional consequences that can be negatively modulated by long-term inhibition of NOS activity. (Am J Pathol 2003, 162:1985-1993)

关键词：主动脉腹/药物作用主动脉腹/病理学主动脉腹/病理生理学主动脉胸/药物作用主动脉胸/病理学主动脉胸/病理生理学动脉/药物作用动脉/病理学动脉/病理生理学腹水/酶学腹水/病理生理学血液循环/药物作用内皮血管/药物作用内皮血管/病理学内皮血管/病理生理学酶抑制剂/药理学纤维化肠系膜动脉/药物作用肠系膜动脉/病理学肠系膜动脉/病理生理学 NG-硝基精氨酸甲酯/药理学一氧化氮合酶/拮抗剂和抑制剂一氧化氮合酶/代谢一氧化氮合酶Ⅲ型大鼠 Wistar 肾动脉/药物作用肾动脉/病理学肾动脉/病理生理学血管中膜/药物作用血管中膜/病理学血管中膜/病理生理学动物男(雄)性大鼠

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Design and rationale of the ARBITER trial (Arterial Biology for the Investigation of the Treatment Effects of Reducing Cholesterol) - A randomized trial comparing the effects of atorvastatin and pravastatin on carotid artery intima-media thickness

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AMERICAN HEART JOURNAL 2001年第3期141卷 342-347页

作者： Markwood, TT Kent, SM Coyle, LC Flaherty, PJ O'Malley, PG Taylor, AJ Walter Reed Army Med Ctr Serv Cardiol Dept Med Washington DC 20307 USA Walter Reed Army Med Ctr Gen Internal Med Serv Dept Med Washington DC 20307 USA Uniformed Serv Univ Hlth Sci Bethesda MD 20814 USA

Background As a class, statins ore remarkably effective in reducing low-density lipoprotein (LDL) cholesterol, and several of these drugs have now been shown to reduce coronary heart disease morbidity and mortality. However, several important controversies in the use of statins remain to be answered by clinical trials. For example, it is controversial whether marked cholesterol reduction to levels below 100 mg/dL would further reduce the incidence of coronary heart disease. Furthermore, concerns about differences among statins for nonlipid effects has raised the concern that the assumption of: a class effect is premature until head-to-heed clinical trials are completed. Methods Arterial Biology for the investigation for the Treatment Effects of Reducing Cholesterol (ARBITER) is a single-center, randomized, active-controlled study comparing the efficacy of high-dose atorvastatin (80 mg/d) and pravastatin (40 mg/d) in patients being treated for either the primary or secondary prevention of coronary heart disease. This trial will enroll up to 200 patients For the primary end point of the mean change in intima-media thickness of the common carotid artery. This effect will be evaluated over a treatment duration of 12 months. Secondary end points include the effects of statin therapy on inflammatory and hemostatic markers (C-reactive protein and fibrinogen). Conclusion ARBITER will provide important date on the role of marked LDL reduction and the "class effect" theory of statin therapy in cardiovascular medicine.

关键词：颈总动脉/药物作用颈总动脉/病理学胆固醇 LDL/分析冠心病/药物疗法冠心病/病理学庚酸类/药理学庚酸类/治疗应用羟甲基戊二酰基CoA还原酶类/药理学羟甲基戊二酰基CoA还原酶类/治疗应用普伐他丁/药理学普伐他丁/治疗应用吡咯类/药理学吡咯类/治疗应用研究设计血管内膜/药物作用血管内膜/病理学血管中膜/药物作用血管中膜/病理学人类

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Effects of hydroxymethylglutaryl coenzyme A reductase inhibitor simvastatin on smooth muscle cell proliferation in vitro and neointimal formation in vivo after vascular injury

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JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY 2000年第1期35卷 214-221页

作者： Indolfi, C Cioppa, A Stabile, E Di Lorenzo, E Esposito, G Pisani, A Leccia, A Cavuto, L Stingone, AM Chieffo, A Capozzolo, C Chiariello, M Univ Naples Federico II Div Cardiol Lab Intervent Cardiol I-80131 Naples Italy

OBJECTIVES We sought to evaluate the effects of hydroxymethylglutaryl coenzyme A (HMG-CoA) reductase inhibitors on vascular smooth muscle cell (VSMC) proliferation in vitro and neointimal formation in vivo after vascular injury. BACKGROUND Neointimal hyperplasia after vascular injury is responsible for restenosis after arterial stenting, whereas arterial remodeling and neointimal formation are the causes of restenosis after percutaneous transluminal coronary angioplasty. METHODS We assessed the effect of simvastatin on in vitro VSMC proliferation. To study the effects of simvastatin in vivo, balloon injury and stent deployment were performed in the common carotid artery of rats. Neointimal area was measured two weeks later in the balloon injury model and three weeks after stent deployment. RESULTS Simvastatin markedly inhibits VSMC proliferation in vitro. In vivo, simvastatin reduced, in a dose-dependent manner, the neointimal area and the neointima-media ratio after balloon injury from 0.266 +/- 0.015 mm(2) to 0.080 +/- 0.026 mm(2) and from 1.271 +/- 0.074 to 0.436 +/- 0.158 (p < 0.001 vs. control rats) at the highest dose. Simvastatin also significantly reduced the neointimal formation and the neointima-media ratio after stenting from 0.508 +/- 0.035 mm(2) to 0.362 +/- 0.047 mm(2) (p < 0.05 vs. control rats) and from 2.000 +/- 0.136 to 1.374 +/- 0.180 (p < 0.05 vs. control rats). The vessel thrombosis rate after stent deployment was 30% in the control group and 11.1% in the treated group (p = NS). Moreover, the systemic administration of simvastatin did not affect hepatic and renal functions, blood pressure or heart rate. CONCLUSIONS Simvastatin potently inhibits VSMC proliferation in vitro and reduces neointimal formation in a rat model of vascular injury. (C) 1999 by the American College of Cardiology.

关键词：细胞分裂/药物作用细胞分裂/生理学细胞培养的移植物闭塞血管/病理学羟甲基戊二酰基CoA还原酶抑制剂/药理学肌平滑血管/药物作用肌平滑血管/病理学大鼠 Wistar 复发斯伐他汀/药理学支架血管内膜/药物作用血管内膜/病理学血管中膜/药物作用血管中膜/病理学伤口愈合/药物作用伤口愈合/生理学动物男(雄)性大鼠

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Arterial responses in vitro and plasma digoxin immunoreactivity after losartan and enalapril treatments in experimental hypertension

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PHARMACOLOGY & TOXICOLOGY 2000年第1期86卷 36-43页

作者： Kalliovalkama, J Kähönen, M Tolvanen, JP Wu, XM Voipio, J Pekki, A Doris, PA Ylitalo, P Pörsti, I Univ Tampere Sch Med Dept Pharmacol Sci FIN-33101 Tampere Finland Univ Tampere Sch Med Dept Anat FIN-33101 Tampere Finland Tampere Univ Hosp Dept Clin Physiol Tampere Finland Tampere Univ Hosp Dept Clin Chem FIN-33521 Tampere Finland Tampere Univ Hosp Dept Internal Med Tampere Finland Univ Helsinki Dept Biosci Div Anim Physiol FIN-00014 Helsinki Finland Univ Texas Hlth Sci Ctr Inst Mol Med Houston TX USA

Treatment with the angiotensin-converting enzyme inhibitor, quinapril, has been shown to normalize increased dihydropyridine sensitivity and impaired potassium relaxation, characteristic features of arterial smooth muscle in spontaneously hypertensive rats, and also reduce the concentration of plasma digoxin-like immunoreactivity in these animals. However, whether angiotensin II receptor blocker therapy can beneficially influence these variables is not known. Therefore, we compared the effects of 10-week losartan and enalapril treatments (15 and 4 mg/kd/day, respectively) on functional responses of mesenteric arterial rings in spontaneously hypertensive rats and Wistar-Kyoto rats. Both losartan and enalapril normalized blood pressure, cardiac mass, and media to lumen ratio without significantly changing the media cross-sectional area in the mesenteric artery of spontaneously hypertensive rats (i.e. induced outward remodelling). The inhibitory effect of the calcium entry blocker nifedipine on calcium-evoked contractions was similar and less marked in arterial preparations from Wistar-Kyoto rats and losartan- and enalapril-treated spontaneously hypertensive rats than in those from untreated spontaneously hypertensive rats. Furthermore, the relaxations of arterial rings induced by the return of potassium to the organ bath (upon precontractions elicited by potassium-free solution) were used to evaluate the function of vascular Na+,K+-ATPase. The rate of potassium relaxation was faster in losartan- and enalapril-treated spontaneously hypertensive rats and all Wistar-Kyoto groups than in untreated spontaneously hypertensive rats, and the response was effectively inhibited by the sodium pump inhibitor ouabain. Both treatments especially augmented the ouabain-sensitive part of the potassium-relaxation in spontaneously hypertensive rats, indicating the involvement of the sodium pump in this response. However, no significant changes in plasma digoxin-like immunoreactivity wer

关键词：血管紧张素受体拮抗剂血管紧张素转换酶抑制药/药理学抗高血压药/药理学血压体重/药物作用心脏扩大/预防和控制地高辛/血液地高辛/免疫学二氢吡啶类/药理学依那普利/药理学心脏/解剖学和组织学高血压/血液高血压/药物疗法洛沙坦/药理学肠系膜动脉/药物作用肠系膜动脉/生理学肌平滑血管/药物作用肌平滑血管/病理生理学硝苯地平/药理学器官测量/药物作用氯化钾/药理学大鼠近交SHR 大鼠近交WKY 受体血管紧张素 1型受体血管紧张素 2型钠钾交换ATP酶/生理学血管中膜/药物作用动物男(雄)性大鼠

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Regulation of myosin-bound protein phosphatase by insulin in vascular smooth muscle cells: Evaluation of the role of Rho kinase and phosphatidylinositol-3-kinase-dependent signaling pathways

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MOLECULAR ENDOCRINOLOGY 2000年第9期14卷 1365-1376页

作者： Begum, N Duddy, N Sandu, O Reinzie, J Ragolia, L Winthrop Univ Hosp Diabet Res Lab Mineola NY 11501 USA SUNY Stony Brook Sch Med Stony Brook NY 11794 USA

In this study, we examined the molecular mechanism of myosin-bound protein phosphatase (MBP) regulation by insulin and evaluated the role of MBP in insulin-mediated vasorelaxation. Insulin rapidly stimulated MBP in confluent primary vascular smooth muscle cell (VSMC) cultures. In contrast, VSMCs isolated from diabetic and hypertensive rats exhibited impaired MBP activation by insulin. Insulin-mediated MBP activation was accompanied by a rapid time-dependent reduction in the phosphorylation state of the myosin-bound regulatory subunit (MBS) of Map. The decrease observed in MBS phosphorylation was due to insulin-induced inhibition of Rho kinase activity. Insulin also prevented a thrombin-mediated increase in Rho kinase activation and abolished the thrombin-induced increase in MBS phosphorylation and MBP inactivation. These data are consistent with the notion that insulin inactivates Rho kinase and decreases MBS phosphorylation to activate MBP in VSMCs. Furthermore, treatment with synthetic inhibitors of phosphatidylinositol-3 kinase (PI3-kinase), nitric oxide synthase (NOS), and cyclic guanosine monophosphate (cGMP) all blocked insulin's effect on MBP activation. We conclude that insulin stimulates MBP via its regulatory subunit, MBS partly by inactivating Rho kinase and stimulating NO/cGMP signaling via PI3-kinase as part of a complex signaling network that controls 20-kDa myosin light chain (MLC20) phosphorylation and VSMC contraction.

关键词： 1-磷脂酰肌醇3-激酶/代谢雄二烯类/药理学主动脉/细胞学主动脉/药物作用主动脉/生理学细胞培养的糖尿病 2型/病理生理学酶激活酶抑制剂/药理学高血压/病理生理学胰岛素/药理学细胞内信号肽和蛋白质类动力学肌收缩/药物作用肌收缩/生理学肌球蛋白轻链磷酸酶黑软海绵素A/药理学磷酰化蛋白质丝氨酸苏氨酸激酶/代谢大鼠近交WKY 信号传导/药物作用信号传导/生理学凝血酶/药理学血管中膜/细胞学血管中膜/药物作用血管中膜/生理学动物男(雄)性大鼠

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