In adult SHR, chronic ACE inhibition alleviates oxidative stress, nephrosclerosis, proteinuria, and HTN, in part by inhibiting the renal cortical advanced end-product (AGE) mediated pathway, including reductions in AGE, RAGE, Ang II, H2O2, p47phox, NF-kB p65, phosphorylated NF-kB p65, vascular cell adhesion molecule (VCAM)-1 and TGF-β1 [217]. Here, NFKB1 is linked to hypertensive disorder.