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. Author manuscript; available in PMC: 2012 Jan 1.
Published in final edited form as: Curr Opin Nephrol Hypertens. 2011 Jan;20(1):37–43. doi: 10.1097/MNH.0b013e32834122f1

Figure 1.

Figure 1

Cartoon summarizing data suggesting the endothelium as a “salt sensor” that responds to changes in [Na+], [K+] and flow by altering production of TGF-β, a fibrogenic growth factor that modifies endothelial and smooth muscle function and promotes vascular stiffness, and NO, a vasodilator that also serves as a potential countervailing influence on TGF-β. Macrophage-derived cytokines, such as VEGF-C and TNF-α, and reactive oxygen species may also directly affect endothelia and vascular smooth muscle and contribute to salt sensitivity. Please see text for details.