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

¹First Department of Medicine, Hamamatsu University School of Medicine, Hamamatsu 431-3192; and ²Medical Center, Shizuoka University, Shizuoka 422-8529, Japan

Submitted 11 February 2003 ; accepted in final form 7 October 2003

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

dietary salt intake; angiotensin; transforming growth factor-

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