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-beta1 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 (AT1R), and decreased glomerular ANG II type 2 receptor (AT2R), whereas LSI decreased glomerular
TGF-beta1 and TbetaRI and increased glomerular AT2R. CC ameliorated glomerular lesions, reduced glomerular
TGF-beta1 and TbetaRII, and increased glomerular AT2R.
PD-123319 aggravated glomerular lesions and increased glomerular
TGF-beta1 and TbetaRII. Our results suggest that dietary
salt intake influences progression of ATS
nephritis by modulating glomerular
TGF-beta1 and TbetaR expression resulting, at least in part, from altered glomerular AT1R and AT2R expression.