Hypertension (HTN) is associated with increased intestinal permeability and oxidative stress, yet the relationship between gut barrier dysfunction and vascular redox imbalance remains unclear. Berries are rich in polyphenols which are known to enhance antioxidant defenses and preserve tight junction (TJ) integrity. Therefore, the objective of this study was to determine whether a mixed berry (MB) diet initiated prior to hypertensive challenge attenuates angiotensin (Ang) II-induced vascular dysfunction and intestinal barrier disruption, and to characterize the tissue-specific molecular remodeling underlying these effects. Eight-week-old male Sprague-Dawley rats were fed AIN-93M diets (Control, Ang II, Losartan [20 mg/kg]) or AIN-93M supplemented with 10% (w/w) freeze-dried MB (equal parts blackberry, raspberry, blueberry, and strawberry) for 8 weeks. At week 4, osmotic minipumps were implanted to deliver saline (Control) or Ang II (270 ng/kg/min; Ang II, Losartan, MB). Blood pressure (BP) was measured weekly starting at week 4 using tail cuff plethysmography. Vascular function was assessed via wire myography and nitric oxide (NO) metabolites were measured in serum. Intestinal permeability was assessed using FITC-dextran and circulating lipopolysaccharide-binding protein (LBP). TJ proteins, antioxidant enzymes (superoxide dismutase [SOD]1-3, glutathione peroxidase [GPx]1/3), renin-angiotensin system (RAS)-related proteins, and sirtuin 1 (SIRT1) were assessed in the distal colon and aorta over time at weeks 4, 6, and 8. Prior to Ang II infusion, MB supplementation established tissue-specific protective molecular alterations at week 4, including induction of Angiotensin II Type 2 receptor (AT2R) and SIRT1 in distal colon and elevating extracellular antioxidant enzymes SOD3 and GPx3 in aorta. Following Ang II infusion, MB attenuated BP elevations and preserved endothelium-dependent vascular function alongside sustaining elevated circulating NO metabolites. In distal colon, early counter-regulatory RAS engagement led to a robust redox response at week 8. MB supplementation was also associated with a trend toward attenuated intestinal permeability and preserved expression of barrier-associated TJ proteins at week 8. Collectively, these findings demonstrate that MB supplementation initiated prior to hypertensive challenge attenuates Ang II-induced HTN through time-dependent and tissue-specific modulation of the RAS and redox pathways. These findings position whole-food berry supplementation as a complementary therapeutic strategy for mitigating HTN-associated vascular and intestinal dysfunction.