Atrial natriuretic peptide inhibits oxidant-induced increases in endothelial permeability.

Atrial natriuretic peptide inhibits oxidant-induced increases in endothelial permeability.
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心房钠尿肽抑制氧化剂诱导的内皮通透性增加。

DOI:
10.1016/0022-2828(91)90134-8
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发表时间:
1991
影响因子:
5
通讯作者:
Newman,WH
Newman,WH
中科院分区:
医学2区
文献类型:
--
作者:
Lofton,CE;Baron,DA;Heffner,JE;Currie,MG;Newman,WH

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化学和酶促产生的氧化剂改变内皮细胞形状,增加大分子穿过内皮细胞单层的渗透性,并增加肺微血管渗透性。我们研究了心房钠尿肽(ANP)对氧化诱导的牛主动脉内皮细胞单层和离体灌注兔肺损伤的影响。用葡萄糖氧化酶(1.4 U/ml)处理培养的内皮细胞单层引起细胞形状的变化,其特征在于细胞的收缩和形成许多细胞间间隙。葡萄糖氧化酶处理也导致减少F-肌动蛋白应力纤维可视化罗丹明鬼笔环肽荧光。用ANP(10− 7 m)预处理内皮细胞单层(5 min),可减弱氧化剂诱导的细胞形状变化和F-肌动蛋白染色减少。此外,ANP还能显著(P<0.05)降低葡萄糖氧化酶引起的内皮细胞单层对白蛋白通透性的增加。氧化剂诱导的离体灌注兔肺损伤产生肺水肿,测量为肺重量增加。用ANP(10− 7 m)预处理肺可显著抑制体重的增加(P<0.05)。总的来说,这些结果表明,心钠素可能采取行动,以保护内皮屏障功能,减少水肿形成所造成的氧化损伤。
Chemically and enzymatically generated oxidants alter endothelial cell shape, increase macromolecular permeability across endothelial cell monolayers, and increase lung microvascular permeability. We examined the effect of ANP (atrial natriuretic peptide) on oxidant-induced injuries to bovine aortic endothelial cell monolayers and to isolated, perfused rabbit lungs. Treatment of cultured endothelial monolayers with glucose oxidase (1.4 U/ml) caused changes in cell shape characterized by a retraction of cells and the formation of numerous intercellular gaps. Glucose oxidase treatment also caused a reduction in F-actin stress fibers visualized by rhodamine-phalloidin fluorescence. Pretreatment (5 min) of the endothelial monolayers with ANP (10−7m) attenuated the oxidant-induced changes in cell shape and reduction in F-actin staining. In addition, ANP significantly (P<0.05) reduced increases in endothelial monolayer permeability to albumin resulting from glucose oxidase treatment. Oxidant-induced injury of isolated, perfused rabbit lungs produced pulmonary edema measured as an increase in lung weight. This increase in weight was significantly (P<0.05) inhibited by pretreatment of lungs with ANP (10−7m). Collectively, these results suggest that ANP may act to preserve endothelial barrier function and reduce edema formation caused by oxidant injury.
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