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首页> 外文期刊>Thrombosis and Haemostasis: Journal of the International Society on Thrombosis and Haemostasis >Angiotensin II enhances thrombosis development in renovascular hypertensive rats.
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Angiotensin II enhances thrombosis development in renovascular hypertensive rats.

机译:血管紧张素II增强肾血管性高血压大鼠的血栓形成。

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摘要

There is an increased number of in vitro evidence that angiotensin II (Ang II) may promote thrombosis. However there are no in vivo experiments exploring the effect of Ang II on thrombus formation. In the present study we have investigated the influence of Ang II on venous thrombosis in renovascular hypertensive rats. Furthermore, we examined the role of AT(1) receptor and Ang II metabolites: angiotensin III (Ang III) and angiotensin IV (Ang IV) in the mechanisms of Ang II action. The contribution of coagulation and fibrinolytic systems in the mode of Ang II action was also determined. Venous thrombosis was induced by ligation of vena cava. Ang II infused into rats developing venous thrombosis caused dose-dependent increase in thrombus weight, which was partially reversed by losartan, selective AT(1) antagonist. Ang III did not influence the thrombus formation in hypertensive rats, while Ang IV caused a marked increase in thrombus weight only in one of the used doses. Our study shows that Ang II via AT(1) receptor enhances thrombosis development. The prothrombotic effect of Ang II may partially depend on enhanced leukocytes adhesion to endothelial cells accompanied by accelerated fibrin formation and increased plasma level of PAI-1. Moreover, Ang II action is partially mediated by one of its metabolites - Ang IV.
机译:越来越多的体外证据表明,血管紧张素II(Ang II)可能会促进血栓形成。但是,尚无体内实验探讨Ang II对血栓形成的影响。在本研究中,我们研究了血管紧张素Ⅱ对肾血管性高血压大鼠静脉血栓形成的影响。此外,我们检查了AT(1)受体和Ang II代谢产物的作用:Ang II作用机制中的血管紧张素III(Ang III)和血管紧张素IV(Ang IV)。还确定了凝血和纤溶系统在Ang II作用模式中的贡献。静脉腔静脉结扎诱发静脉血栓形成。向发生静脉血栓形成的大鼠中注入Ang II会导致血栓重量呈剂量依赖性增加,而洛沙坦(选择性AT(1)拮抗剂)可部分逆转血栓重量。 Ang III不会影响高血压大鼠的血栓形成,而Ang IV仅以一种使用剂量引起血栓重量显着增加。我们的研究表明,Ang II通过AT(1)受体增强了血栓形成的发展。 Ang II的血栓形成作用可能部分取决于白细胞与内皮细胞的粘附增强,伴随着加速的血纤蛋白形成和PAI-1血浆水平升高。此外,Ang II的作用部分地由其一种代谢产物Ang IV介导。

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