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1
Nephrology Research and Training Center, Comprehensive Cancer Center, and Cell Adhesion and Matrix Research Center, Division of Nephrology, Department of Medicine and Department of Physiology and Biophysics, University of Alabama at Birmingham, 35294-0007; and Department of Veterans Affairs Medical Center, Birmingham, Alabama 35233
Dietary salt controls production of nitric oxide (NO), a potent
paracrine relaxation factor involved in glomerular filtration and salt
excretion. We hypothesized that glomerular NO production was enhanced
through endothelial nitric oxide synthase (NOS3). Rats in metabolic
cages were studied after 4 days on 0.3% (Lo-salt) or 8.0% (Hi-salt)
NaCl diet. Steady-state mRNA and protein levels of NOS3 and
calcium-dependent NO production of isolated glomeruli from Hi-salt
animals were greater than those values observed in glomeruli from
Lo-salt rats. Because dietary salt enhanced glomerular production of
transforming growth factor-
1 (TGF-1) [W.-Z. Ying and P. W. Sanders. Am. J. Physiol. 274 (Renal Physiol. 43): F635-F641, 1998], studies were then conducted to examine the interaction between NOS3 and TGF-1. Glomerular steady-state levels of mRNA of
NOS3 and TGF-1 directly correlated
(r2 = 0.946;
P < 0.0001). A neutralizing antibody
to TGF- reduced NOS3 protein and NO production in cultured glomeruli
from Hi-salt animals to levels seen in the Lo-salt glomeruli. Thus
dietary salt increased glomerular expression of TGF-1, which in turn augmented NO production through NOS3.
sodium chloride; nitric oxide; glomerulus; endothelial nitric oxide
synthase; transforming growth factor-1
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