Dietary salt increases endothelial nitric oxide synthase and TGF-beta1 in rat aortic endothelium.

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-beta1 (TGF-beta1) production. We hypothesized that dietary NaCl intake regulated expression of the endothelial isoform of nitric oxide synthase (NOS3) and TGF-beta1 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-beta1 in aortas of rats on 8.0% NaCl diet. By ELISA, both total and active TGF-beta1 were increased in these vessel segments. Endothelial denudation of aortic rings reduced active TGF-beta1 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-beta1 expression in the arterial wall; NOS3 expression was at least partially regulated by endothelial cell production of TGF-beta1.