Male 4-week-old SD rats were randomly divided into 4 groups (n=8): Normal group (Con)， model group (BP)， captopril group (Cap， 10 mg/kg captopril)， and Prinsepia utilis Royle peptide NLPLL intervention group (PP， 10 mg/kg NLPLL). Except for the normal group， which was fed ordinary feed and normal drinking water， the other groups were fed 20% fructose water and 8% high-salt feed. The model was established for 8 weeks， and the intervention was conducted for 8 weeks. The results showed that NLPLL increased the activity of superoxide dismutase (SOD) and catalase (CAT)， increased glutathione (GSH) content and total antioxidant capacity， and reduced the production of malondialdehyde (MDA) in kidney tissue， thereby reducing the oxidative damage to rat kidneys caused by high fructose and high salt. Alleviating the inflammatory response in the kidneys of hypertensive rats by reducing the levels of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) and increasing the levels of the anti-inflammatory factor interleukin-10 (IL-10). NLPLL could exert antihypertensive effect by increasing the activity of NO and eNOS， and decreasing the levels of renin， ACE， Ang II， AT1R and PRR， and reducing renal interstitial fibrosis and inflammatory cell infiltration. NLPLL formed nine hydrogen bonds with six amino acid residues of ACE， including three key active site residues of ACE (Gln281， Lys511， and Tyr520). Additionally， NLPLL forms three hydrogen bonds with two residues of AT1R. In summary， NLPLL could reduce blood pressure in rats with dietary hypertension induced by high fructose and high salt， and by reducing oxidative damage and inflammation in the kidney， increasing NO and eNOS activities， and regulating the levels of key enzymes and molecules of the renin-angiotensin system， improve kidney damage caused by dietary hypertension. This study could provide a theoretical basis for the improvement of diet-induced hypertension and renal tissue damage by Prinsepia utilis Royle peptide and the development of natural antihypertensive functional factors.