The induction and activation of endothelial nitricoxide synthase (eNOS) by PKC increases the availability of nitric oxide (NO) indiabetic kidney in the first stages of DKD.32 Increased NO contributes to elevation of prostaglandinE1 levels, Ang II activity, and activation of the vascular endothelial growthfactor (VEGF), resulting in increased permeability, endothelial dysfunction,glomerular hyperfiltration and albuminuria.33,34. Here, AGT is linked to endothelial dysfunction.