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AngiotensinⅡis involved in nitric oxide synthase and cyclo-oxygenase inhibition-induced leukocyte-endothelial cell interactions in vivo

机译:血管紧张素Ⅱ在体内参与一氧化氮合酶和环加氧酶抑制诱导的白细胞-内皮细胞相互作用

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摘要

Chronic inhibition of nitric oxide synthase(NOS)provokes a hypertensive state which has been shown to be angiotensinⅡ(Ang-Ⅱ)dependent. In addition to raising blood pressure, NOS inhibition also causes leukocyte adhesion. The present study was designed to define the role of Ang- Ⅱin hypertension and in the leukocyte-endothelial cell interactions induced by acute NOS or cyclo- oxygenase(COX)inhibition using inntravital microscopy within the rat mesenteric microcirculation. While pretreatment with an Ang-ⅡAT_1 receptor antagonist(losartan)reversed the prompt Increase in mean arterial blood pressure(MABP)caused by indomethacin, it had no effect on the Increase evoked by systemic L-NAME administration.
机译:长期抑制一氧化氮合酶(NOS)会导致高血压状态,已显示它是血管紧张素Ⅱ(Ang-Ⅱ)依赖性的。除了提高血压外,抑制NOS还会引起白细胞粘附。本研究旨在通过玻璃体内镜在大鼠肠系膜微循环中确定Ang-Ⅱ在高血压以及急性NOS或环氧化酶(COX)抑制诱导的白细胞-内皮细胞相互作用中的作用。尽管用Ang-ⅡAT_1受体拮抗剂洛沙坦逆转了吲哚美辛引起的平均动脉血压(MABP)的迅速升高,但对全身性L-NAME给药引起的升高没有影响。

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