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Systemic administration of lipopolysaccharide upregulates angiotensin II expression in rat renal tubules: immunohistochemical and ELISA studies.

机译:脂多糖的全身给药可上调大鼠肾小管中血管紧张素II的表达:免疫组织化学和ELISA研究。

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We investigated whether angiotensin II (AII) peptide is induced in the rat kidney under endotoxemic conditions. Immunohistochemistry revealed strong AII-like immunoreactivity in the renal tubules of rats given high-dose lipopolysaccharide (LPS; 1000 microg/kg) intraperitoneally (i.p.). AII-like immunoreactivity in renal tubules was slight at 1h after the LPS injection, but marked at 3 h. There were few signals in the kidney in saline-injected control rats. When injected at 0.1, 10, or 1000 microg/kg i.p., LPS-induced a dose-related increase in AII-like immunoreactivity in renal tubules that was unaffected by treatment with the prostaglandin-synthesis blocker indomethacin. ELISA measurement of the AII concentration in the whole kidney supported the above findings. These results suggest that systemically administered LPS induces AII peptide expression in renal tubules by a prostaglandin-independent mechanism.
机译:我们调查了内毒素血症条件下大鼠肾脏是否诱导了血管紧张素II(AII)肽。免疫组织化学显示,腹膜内(i.p.)给予高剂量脂多糖(LPS; 1000 microg / kg)的大鼠肾小管具有很强的AII样免疫反应性。在LPS注射后1小时,肾小管中的AII样免疫反应轻微,但在3小时时显着。注射盐水的对照大鼠的肾脏中几乎没有信号。当以0.1、10或1000 microg / kg i.p.腹腔注射时,LPS诱导肾小管中剂量相关的AII样免疫反应性增加,而不受前列腺素合成阻滞剂消炎痛的影响。整个肾脏中AII浓度的ELISA测量支持了上述发现。这些结果表明,全身给药的LPS通过前列腺素非依赖性机制诱导肾小管中的AII肽表达。

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