Secreted protein acidic and rich in cysteine (SPARC) is reported to induce collagen deposition through a disintegrin and metalloproteinase with thrombospondin type 1 motif (ADAMTS1) production and promote pro-inflammatory cytokine release in aging myocardium. The present study investigated the roles for SPARC in vascular endothelial cell dysfunction and inflammation using deoxycorticosterone acetate (DOCA)-salt hypertensive rats and cultured aortic endothelial cells. DOCA-salt treatment increased systolic blood pressure in 2 weeks and induced further hypertensin in 3 weeks. Acetylcholine-induced vasodilatory response impaired and macrophage infiltration increased in DOCA-salt rat aortas, both of which showed time-dependent changes. Immunoblot analysis revealed that SPARC and ADAMTS1 expression increased in DOCA-salt rats and peaked at 1 week. Angiotensin II treatment enhanced SPARC and ADAMTS1 protein expression in cultured aortic endothelial cells. Angiotensin II-induced overexpression of LOX-1 and MCP-1 mRNA was further augmented by SPARC or ADAMTS1 gene silencing. In conclusion, SPARC may be induced at the early stage of vascular injury to compensate inflammation. Further investigation into roles for SPARC in inflammation and relationship between SPARC and ADAMTS1 is needed.