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Am J Physiol Heart Circ Physiol 277: H1293-H1298, 1999;
0363-6135/99 $5.00
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Vol. 277, Issue 4, H1293-H1298, October 1999

Dietary salt increases endothelial nitric oxide synthase and TGF-beta 1 in rat aortic endothelium

Wei-Zhong Ying and Paul W. Sanders

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, Birmingham 35294-0007; and Department of Veterans Affairs Medical Center, Birmingham, Alabama 35233

The amount of NaCl in the diet plays an important role in modulating nitric oxide (NO) synthesis in vivo. In the glomerulus, dietary NaCl also regulates transforming growth factor-beta 1 (TGF-beta 1) production. We hypothesized that dietary NaCl intake regulated expression of the endothelial isoform of nitric oxide synthase (NOS3) and TGF-beta 1 in the aorta. Administration of 8.0% NaCl diet to rats for 7 days did not affect blood pressure but increased steady-state mRNA and protein levels of NOS3 in the arterial wall compared with animals on 0.3% NaCl diet. Northern analysis demonstrated increased steady-state amounts of mRNA of TGF-beta 1 in aortas of rats on 8.0% NaCl diet. By ELISA, both total and active TGF-beta 1 were increased in these vessel segments. Endothelial denudation of aortic rings reduced active TGF-beta 1 secretion to undetectable levels. Addition of a neutralizing antibody to TGF-beta to aortic ring segments attenuated NO production but not to that observed in animals on the 0.3% NaCl diet. The data showed that dietary NaCl intake modulated NOS3 and TGF-beta 1 expression in the arterial wall; NOS3 expression was at least partially regulated by endothelial cell production of TGF-beta 1.

transforming growth factor-beta 1; nitric oxide; sodium chloride; Sprague-Dawley rat


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