A chronic NOS/NO inhibition model of HTN in rats shows that activated RAAS (renin–angiotensin–aldosterone system) in the renal cortex is linked to the upregulation of TGF-β1 and fibronectin, which are significant factors producing renal injury (glomerulosclerosis, proteinuria, and interstitial fibrosis) [34,35]. Here, TGFB1 is linked to hypertensive disorder.