Dietary salt enhances glomerular endothelial nitric oxide synthase through TGF-beta1.
Dietary salt enhances glomerular endothelial nitric oxide synthase through TGF-beta1.
复制标题
膳食盐通过 TGF-β1 增强肾小球内皮一氧化氮合酶。
DOI：
10.1152/ajprenal.1998.275.1.f18
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发表时间：
1998
期刊：
影响因子：
--
通讯作者：
Sanders,PW
中科院分区：
文献类型：
--
作者：
Ying,WZ;Sanders,PW
膳食盐控制一氧化氮（NO）的产生，一氧化氮是一种参与肾小球滤过和盐排泄的有效旁分泌松弛因子。我们假设肾小球NO的产生是通过内皮型一氧化氮合酶（NOS 3）增强的。代谢笼中的大鼠在4天后进行了研究，0.3%（低盐）或8.0%（高盐）NaCl饮食。稳态的mRNA和蛋白质水平的NOS 3和钙依赖性NO生产的高盐动物离体肾小球大于从低盐大鼠肾小球中观察到的值。由于饮食中的盐增加了肾小球转化生长因子-β1（TGF-β1）的产生[W. Z. Ying和P.W. Sanders.Am. J.Physiol.274（Renal Physiol.43）：F635-F641，1998]，然后进行研究以检查NOS 3和TGF-β1之间的相互作用。肾小球稳态NOS 3和TGF-β1 mRNA水平呈正相关（r2= 0.946;P< 0.0001）。TGF-β的中和抗体将高盐动物培养的肾小球中NOS 3蛋白和NO的产生降低至低盐肾小球中的水平。因此，膳食盐增加了肾小球TGF-β1的表达，这反过来又通过NOS 3增加了NO的产生。
Dietary salt controls production of nitric oxide (NO), a potent paracrine relaxation factor involved in glomerular filtration and salt excretion. We hypothesized that glomerular NO production was enhanced through endothelial nitric oxide synthase (NOS3). Rats in metabolic cages were studied after 4 days on 0.3% (Lo-salt) or 8.0% (Hi-salt) NaCl diet. Steady-state mRNA and protein levels of NOS3 and calcium-dependent NO production of isolated glomeruli from Hi-salt animals were greater than those values observed in glomeruli from Lo-salt rats. Because dietary salt enhanced glomerular production of transforming growth factor-β1 (TGF-β1) [W.-Z. Ying and P. W. Sanders.Am. J. Physiol.274 (Renal Physiol. 43): F635–F641, 1998], studies were then conducted to examine the interaction between NOS3 and TGF-β1. Glomerular steady-state levels of mRNA of NOS3 and TGF-β1 directly correlated (r2= 0.946;P< 0.0001). A neutralizing antibody to TGF-β reduced NOS3 protein and NO production in cultured glomeruli from Hi-salt animals to levels seen in the Lo-salt glomeruli. Thus dietary salt increased glomerular expression of TGF-β1, which in turn augmented NO production through NOS3.