Dietary salt intake modulates progression of antithymocyte serum nephritis through alteration of glomerular angiotensin II receptor expression
Dietary salt intake modulates progression of antithymocyte serum nephritis through alteration of glomerular angiotensin II receptor expression
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DOI：
10.1152/ajprenal.00059.2003
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发表时间：
2004-02-01
影响因子：
4.2
通讯作者：
Hishida, A
中科院分区：
文献类型：
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作者：
Suzuki, H;Yamamoto, T;Hishida, A
膳食盐摄入量调节肾素-血管紧张素系统（RAS）；然而，人们对盐摄入量对肾小球肾炎进展的影响知之甚少。我们研究了正常（NSI）、低盐（LSI）和高盐摄入（HSI）的抗胸腺细胞血清（ATS）肾炎大鼠以及接受坎地沙坦西酯（CC）的HSI大鼠和接受PD-123319的LSI大鼠的肾小球中TGF-β（1）I型（TbetaRI）和II型（TbetaRII）TGF-β受体和RAS成分的表达。与 NSI 组相比，LSI 组大鼠肾小球病变较轻，HSI 组大鼠肾小球病变加重。 LSI 大鼠的肾内肾素和肾小球 ANG II 水平显着较高，HSI 大鼠的肾内肾素和肾小球 ANG II 水平显着较低。在 ATS 肾炎中，HSI 增加肾小球 TbetaRI、TbetaRII 和 ANG II 1 型受体 (AT(1)R)，并减少肾小球 ANG II 2 型受体 (AT(2)R)，而 LSI 减少肾小球 TGF-β(1) 和 TbetaRI，并增加肾小球 AT(2)R。 CC改善肾小球病变，减少肾小球TGF-β(1)和TbetaRII，并增加肾小球AT(2)R。 PD-123319 加重肾小球病变并增加肾小球 TGF-β(1) 和 TbetaRII。我们的结果表明，膳食盐摄入量通过调节肾小球 TGF-β(1) 和 TbetaR 表达来影响 ATS 肾炎的进展，这至少部分是由于肾小球 AT(1)R 和 AT(2)R 表达的改变所致。
Dietary salt intake modulates the renin-angiotensin system (RAS); however, little is known about the effect of salt intake on the progression of glomerulonephritis. We investigated the glomerular expression of TGF-beta(1) type I (TbetaRI) and II (TbetaRII) TGF-beta receptors and RAS components in rats with antithymocyte serum (ATS) nephritis on normal (NSI)-, low (LSI)-, and high-salt intake (HSI) and on HSI rats receiving candesartan cilexetil ( CC) and LSI rats receiving PD-123319. Glomerular lesions were less severe in rats on LSI and aggravated in those on HSI compared with those on NSI. Intrarenal renin and glomerular ANG II levels were significantly higher in LSI and lower in HSI rats. In ATS nephritis, HSI increased glomerular TbetaRI, TbetaRII, and ANG II type 1 receptor (AT(1)R), and decreased glomerular ANG II type 2 receptor (AT(2)R), whereas LSI decreased glomerular TGF-beta(1) and TbetaRI and increased glomerular AT(2)R. CC ameliorated glomerular lesions, reduced glomerular TGF-beta(1) and TbetaRII, and increased glomerular AT(2)R. PD-123319 aggravated glomerular lesions and increased glomerular TGF-beta(1) and TbetaRII. Our results suggest that dietary salt intake influences progression of ATS nephritis by modulating glomerular TGF-beta(1) and TbetaR expression resulting, at least in part, from altered glomerular AT(1)R and AT(2)R expression.