The present study examined the effect and part mechanism of angiotensin II–stimulated integrin β 3 gene expression in human umbilical vein endothelial cells. Protein level and mRNA level of integrin β 3 expression were determined using enzyme-linked immunoadsorbent assay and reverse transcription–polymerase chain reaction. Four plasmids of 5′-different deletion of integrin β 3 gene promoter were constructed to transiently transfected into cells to uncover the region in response to angiotensin II. Blockade of nuclear factor-κB (NF-κB) signaling pathway effect on integrin β 3 expression was analyzed by cotransfection with mutant plasmids for NF-κB–inducing kinase, inhibitory proteins α and β of NF-κB kinase, respectively, together with the integrin β 3 plasmid including the sequence -1486 ∼⃒ - 900. The study found that 10 -8 mol/L,10 -7 mol/L, 10 -6 mol/L, and 10 -5 mol/L angiotensin II increased integrin β 3 protein level by 45%, 52%, 62%, and 73% respectively. Angiotensin II at 10 -6 mol/L increased integrin β 3 mRNA level by 67%. The luciferase activity of the integrin β 3 plasmid PGL3 - 1486 ∼⃒ - 900 increased by 84.72% in response to angiotensin II. N -acetylcysteine blocked angiotensin II–induced NF-κB activity and integrin β 3 expression. Blockade of NF-κB signaling pathway abolished the stimulation of angiotensin II. These results suggest that angiotensin II stimulates integrin β 3 expression partly by NF-κB activation. [ABSTRACT FROM AUTHOR]