Inflammation　is　involved　in　pathogenesis　of　hypertension.　NLRP3　inflammasome　activation　is　a　powerful　mediator　of　inflammatory　response　via　caspase-1　activation.　The　present　study　was　designed　to　determine　the　roles　and　mechanisms　of　NLRP3　inflammasome　in　phenotypic　modulation　and　proliferation　of　vascular　smooth　muscle　cells　(VSMCs)　in　hypertension.　Experiments　were　conducted　in　spontaneously　hypertensive　rats　(SHR)　and　primary　aortic　VSMCs.　NLRP3　inflammasome　activation　was　observed　in　the　media　of　aorta　in　SHR　and　in　the　VSMCs　from　SHR.　Knockdown　of　NLRP3　inhibited　inflammasome　activation,　VSMC　phenotypic　transformation　and　proliferation　in　SHR-derived　VSMCs.　Increased　NF　kappa　B　activation,　histone　acetylation　and　histone　acetyltransferase　expression　were　observed　in　SHR-derived　VSMCs　and　in　media　of　aorta　in　SHR.　Chromatin　immunoprecipitation　analysis　revealed　the　increased　histone　acetylation,　p65-NF　kappa　B　and　Pol　II　occupancy　at　the　NLRP3　promoter　in　vivo　and　in　vitro.　Inhibition　of　NF　kappa　B　with　BAY11-7082　or　inhibition　of　histone　acetyltransferase　with　curcumin　prevented　the　NLRP3　inflammasome　activation,　VSMC　phenotype　switching　and　proliferation　in　VSMCs　from　SHR.　Moreover,　curcumin　repressed　NF　kappa　B　activation.　Silencing　of　NLRP3　gene　ameliorated　hypertension,　vascular　remodeling,　NLRP3　inflammasome　activation　and　phenotype　switching　in　the　aorta　of　SHR.　These　results　indicate　that　NLRP3　inflammasome　activation　response　to　histone　acetylation　and　NF　kappa　B　activation　contributes　to　VSMC　phenotype　switching　and　proliferation　and　vascular　remodeling　in　hypertension.