Hypertension is associated with macrovascular and microvascular remodelling. Chronic high blood pressure impacts target organs including the kidney, resulting in proteinuria and impaired perfusion. We have reported that systemic infusion of a P2X7 antagonist reduces blood pressure and increases renal perfusion in a model of ANGII-dependent hypertension (Menzies et al, Kidney International, 2015). In the present study we developed a model of hypertensive vascular remodelling in C57BL/6 mice through a 4-week administration of ANGII (100ng/kg/min) and deoxycorticosterone (DOCA; 50mg), combined with high salt feeding (ANGII DOCA salt; n= 12) versus Sham controls (n=11). ANGII DOCA salt increased systolic blood pressure (ANGII DOCA salt = 136.5±3.2mmHg vs. Sham = 113.3±1.9mmHg; P<0.01) and urinary albumin excretion (ANGII DOCA salt: 357.3±23.2μg/24hr vs. Sham: 22.0±2.1μg/24hr; P<0.0001). Renal histology identified a perivascular fibrosis (ANGII DOCA salt: 54.9±3.7pixels, Sham: 40.2±3.2pixels normalised to vessel thickness; P<0.05). Interstitial fibrosis was not observed. Flow activated cell sorting identified that ANGII DOCA salt caused a 5-fold increase in renal perivascular PDGFRb+ cells, but no change in endothelial, epithelial or macrophage cell types compared with Sham. Immunofluorescence of renal sections colocalised PDGFRb and P2X7 at focal points in the intermediate arterial architecture of the kidney, particularly renal interlobar arteries. These data suggest that perivascular P2X7-expressing cells of the intermediate arteries in the kidney are involved in hypertensive remodelling processes.