Aim To investigate the role of myeloid angiotensin type 1 receptor (Mye AT1R) in vascular insulin resistance and vascular injury in deoxycorticosterone acetate (DOCA)/salt-sensitive hypertensive mice. Methods C57BL/6J mice (wild type, WT) and Mye AT1R－/－ mice were randomly divided into WT group, DOCA/salt-sensitive hypertension group (DOCA group), Mye AT1R－/－group and Mye AT1R－/－/DOCA group, 8 in each group. DOCA/salt-sensitive hypertension was induced by left nephrectomy and DOCA sustained-release tablet implantation. Systolic blood pressure (SBP) was measured by tail cuff method. HE staining was used to observe aortic wall thickness, immunofluorescence was used to detect F4/80 (monocyte/macrophage marker) of aorta, RT-PCR and Western blot were used for mRNA and protein expressions of AT1R, proinflammatory factors and insulin signaling molecules. Acetylcholine or insulin-induced endothelium-dependent vasodilation was determined by isolated vascular perfusion system. Results Compared with WT group, in DOCA group, systolic blood pressure increased by 37%, aortic wall thickness increased by 57%, acetylcholine or insulin-induced endothelium-dependent vasodilation decreased by 32% and 36% respectively (P＜0.05), the number of F4/80 positive cells increased by 195%, the protein expression of monocyte chemoattractant protein-1 (MCP-1), tumor necrosis factor-α (TNF-α) and phosphorylated c-Jun N-terminal kinase (p-JNK) were significantly increased by 42%, 45% and 32% respectively, the protein expression of p-Akt and p-Enos decreased by 36% in the aorta of DOCA mice (P＜0.05). Specific knockout of myeloid AT1R, aortic thickness decreased by 14%, the number of F4/80 positive cells decreased by 44%, acetylcholine or insulin-induced endothelium-dependent vasodilation improved by 21% and 17% respectively, the protein expression of MCP-1, TNF-α and p-JNK decreased by 52%, 41% and 17% respectively, damaged insulin protein PI3K/Akt/eNOS signaling pathway was reversed, the protein expression of p-Akt and p-eNOS increased by 48% and 42% respectively (P＜0.05) without significant reduction in systolic blood pressure. Conclusion Knockout of Mye AT1R can reduce vascular insulin resistance and vascular injury caused by salt-sensitive hypertension, and its mechanism may be related to inhibition of vascular inflammation caused by macrophage infiltration in vascular wall.