Dietary salt intake modulates progression of antithymocyte serum nephritis through alteration of glomerular angiotensin II receptor expression

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Abstract
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-β1type I (TβRI) and II (TβRII) TGF-β 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 TβRI, TβRII, and ANG II type 1 receptor (AT1R), and decreased glomerular ANG II type 2 receptor (AT2R), whereas LSI decreased glomerular TGF-β1and TβRI and increased glomerular AT2R. CC ameliorated glomerular lesions, reduced glomerular TGF-β1and TβRII, and increased glomerular AT2R. PD-123319 aggravated glomerular lesions and increased glomerular TGF-β1and TβRII. Our results suggest that dietary salt intake influences progression of ATS nephritis by modulating glomerular TGF-β1and TβR expression resulting, at least in part, from altered glomerular AT1R and AT2R expression.