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Am J Physiol Renal Physiol (October 14, 2003). doi:10.1152/ajprenal.00059.2003
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Submitted on February 11, 2003
Accepted on October 7, 2003

Dietary salt intake modulates progression of anti-thymocyte serum nephritis through alteration of glomerular angiotensin II receptor expression

Hiroyuki Suzuki1*, Tatsuo Yamamoto1, Naoki Ikegaya2, and Akira Hishida1

1 First Department of Medicine, Hamamatsu University School of Medicine, Hamamatsu, Shizuoka, Japan
2 Medical Center, Shizuoka University, Shizuoka, Shizuoka, Japan

* To whom correspondence should be addressed. E-mail: hirosuzu{at}hama-med.ac.jp.

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, types I (T{beta}RI) and II (T{beta}RII) TGF-{beta} receptors, and RAS components in rats with anti-thymocyte serum (ATS) nephritis on normal (NSI), low (LSI), and high salt intake (HSI), and on HSI receiving candesartan cilexetil (CC) and LSI receiving PD123319. Glomerular lesions were less severe in rats on LSI and aggravated in those on HSI than NSI. Intrarenal renin and glomerular angiotensin II (AII) levels were significantly higher in LSI and lower in HSI rats. In ATS nephritis, HSI increased glomerular T{beta}RI, T{beta}RII, and AII type 1 receptor (AT1-R), and decreased glomerular AII type 2 receptor (AT2-R), while LSI decreased glomerular TGF-{beta}1 and T{beta}RI, and increased glomerular AT2-R. CC ameliorated glomerular lesions, reduced glomerular TGF-{beta}1 and T{beta}RII, and increased glomerular AT2-R. PD123319 aggravated glomerular lesions, and increased glomerular TGF-{beta}1 and T{beta}RII. Our results suggest that dietary salt intake influences progression of ATS nephritis by modulating glomerular TGF-{beta}1 and T{beta}R expression resulting from, at least in part, altered glomerular AT1-R and AT2-R expression.




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