Dietary salt modulates renal production of transforming growth factor-beta in rats.
Dietary salt modulates renal production of transforming growth factor-beta in rats.
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DOI：
10.1152/ajprenal.1998.274.4.f635
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发表时间：
1998-04
期刊：
影响因子：
--
通讯作者：
W. Ying;P. Sanders
中科院分区：
文献类型：
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作者：
W. Ying;P. Sanders
转化生长因子是一种强大的多功能多肽，与肾功能和肾小球硬化有关。我们推测，饮食盐改变了肾脏转化生长因子-β的产生。随着饮食盐的增加，大鼠肾脏中转化生长因子-β1、-β2和-β3的mRNA的稳态水平持续增加。在血清转化生长因子-β1浓度没有变化的情况下，8.0%氯化钠饮食增加了尿中转化生长因子-β1的排泄量，表明肾脏分泌增加是转化生长因子-β1的来源。在接受8.0%氯化钠饮食的动物中，增加尿流率并不会进一步增加转化生长因子-β1的合成。8.0%的食盐饮食增加了肾小球和肾小管中转化生长因子-β1的产生，尽管活性转化生长因子-β1仅在肾小球中分泌较多。四乙基铵(TEA)可抑制8.0%食盐饮食诱导的肾小球产生非活性和活性的转化生长因子-β1，而不是格列本脲。在8.0%的食盐饮食中，心脏产生的转化生长因子-β1也增加，但不受茶叶的影响。结果表明，增加食盐可增加肾小球转化生长因子-β的产生，其机制包括一种茶敏感的钾通道。食盐通过促进肾小球转化生长因子-β的表达，可能直接促进肾小球硬化的发展。
Transforming growth factors (TGF) are potent multifunctional polypeptides that are involved in renal function and glomerular sclerosis. We postulated that dietary salt modified renal production of TGF-beta. An increase in dietary salt produced sustained increases in steady-state levels of mRNA for TGF-beta 1, -beta 2, and -beta 3 in the rat kidney. While serum concentration of TGF-beta 1 did not change, the 8.0% NaCl diet increased urinary excretion of TGF-beta 1, indicating enhanced renal production was the source of TGF-beta 1. Increasing urinary flow rates with diuretics did not further increase synthesis of TGF-beta 1 in animals receiving the 8.0% NaCl diet. The 8.0% NaCl diet increased production of TGF-beta 1 in both glomeruli and tubules, although active TGF-beta 1 was secreted in greater amounts only from glomeruli. Enhanced glomerular production of both inactive and active TGF-beta 1 induced by the 8.0% NaCl diet was inhibited by tetraethylammonium (TEA) and not glybenclamide. Cardiac production of TGF-beta 1 also increased on the 8.0% NaCl diet but was not affected by TEA. The results demonstrated that increased dietary salt augmented glomerular TGF-beta production by a mechanism that included a TEA-sensitive potassium channel. Dietary salt, by facilitating glomerular expression of TGF-beta, may directly promote development of glomerulosclerosis.