醛固酮抑制白细胞介素-1 β诱导的大鼠血管平滑肌细胞一氧化氮合成

Uichi Ikeda , Toshiko Kanbe , Ichiro Nakayama , Yasuhiro Kawahara , Mitsuhiro Yokoyama , Kazuyuki Shimada
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引用次数: 93

摘要

我们研究了醛固酮对血管平滑肌细胞一氧化氮(NO)合成的影响。我们测量了培养的大鼠血管平滑肌细胞中亚硝酸盐(NO的稳定代谢产物)的产生以及诱导型NO合成酶mRNA和蛋白的表达。培养物与白细胞介素-1β(10ng/ml)孵育24小时可显著增加亚硝酸盐的生成。醛固酮以剂量(10−9~10−6M)依赖的方式显著抑制白细胞介素-1β诱导的血管平滑肌细胞产生亚硝酸盐。与白细胞介素-1β孵育12~24小时可引起血管平滑肌细胞中诱导型一氧化氮合酶mRNA的表达,而醛固酮对其表达具有抑制作用。醛固酮还降低了白细胞介素-1β诱导的诱导型一氧化氮合酶蛋白的积累。这些结果表明,醛固酮在白细胞介素-1β刺激的条件下抑制血管平滑肌细胞中NO的合成。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Aldosterone inhibits nitric oxide synthesis in rat vascular smooth muscle cells induced by interleukin-1 β

We investigated the effects of aldosterone on nitric oxide (NO) synthesis in vascular smooth muscle cells. We measured the production of nitrite, a stable metabolite of NO, and the expression of inducible NO synthase mRNA and protein in cultured rat vascular smooth muscle cells. Incubation of the cultures with interleukin-1β (10 ng/ml) for 24 h caused a significant increase in nitrite generation. The interleukin-1β-induced nitrite production by vascular smooth muscle cells was significantly inhibited by aldosterone in a dose (10−9 ∼ 10−6 M)-dependent manner. Incubation with interleukin-1β for 12 ∼ 24 h caused inducible NO synthase mRNA expression in vascular smooth muscle cells, whereas aldosterone had a suppressive effect on its expression. Aldosterone also decreased interleukin-1β-induced inducible NO synthase protein accumulation. These results indicate that aldosterone inhibits NO synthesis under interleukin-1β-stimulated conditions in vascular smooth muscle cells.

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