Protein kinase C (PKC) β is activated under hyperglycemia and in cancerous cells, which has been implicated in cell inflammatory activation. On the other hand, the role of PKCβ in hypertension-associated inflammatory response remains unclear. In this study, we examined the effect of PKCβ inhibitor on angiotensinⅡ (AngⅡ)-induced inflammatory responses in vascular smooth muscle cells. We isolated vascular smooth cells from mesenteric arteries of male Wistar rat. Treatment of vascular smooth muscle cells with Ang II (1-1000 ng/ml) for 15 min increased phosphorylation of PKCβ at the active site at Ser 660 and Thr 641 in dose dependent manner (n=4). Treatment with Ang II (100 ng/ml) for 24 hours increased expression of proliferating cell nuclear antigen (PCNA) and the effect was attenuated by pretreatment with PKCβ inhibitor (LY333531 or CGP53353)(n=6). Also, treatment with Ang II for 48 hours induced cell proliferation and the effect was blocked by pretreatment with the PKCβ inhibitor (n=4). Treatment with Ang II for 24 hours increased reactive oxygen species production and the effect was attenuated by the PKCβ inhibitor (n=4). These results suggest that PKCβ is involved in vascular smooth muscle cell proliferation and oxidative stress in response to Ang II, and may contribute to inflammation associated with hypertension.