Background/Aims:　Angiotensin　(Ang)　II　plays　vital　roles　in　vascular　inflammation　and　remodeling　in　hypertension.　Phenotypic　transformation　of　vascular　smooth　muscle　cells　(VSMCs)　is　a　major　initiating　factor　for　vascular　remodeling.　The　present　study　was　designed　to　determine　the　roles　of　NLRP3　inflammasome　activation　in　Ang　IIinduced　VSMC　phenotypic　transformation　and　vascular　remodeling　in　hypertension.　Methods:　Primary　VSMCs　from　the　aorta　of　NLRP3　knockout　(NLRP3(-/-))　mice　and　wildtype　(WT)　mice　were　treated　with　Ang　II　for　24　h.　Subcutaneous　infusion　of　Ang　II　via　osmotic　minipump　for　2　weeks　was　used　to　induce　vascular　remodeling　and　hypertension　in　WT　and　NLRP3(-/-)　mice.　Results:　NLRP3　gene　deletion　attenuates　Ang　IIinduced　NLRP3　inflammasome　activation,　phenotypic　transformation　from　a　contractile　phenotype　to　a　synthetic　phenotype　and　proliferation　in　primary　mice　VSMCs.　Ang　IIinduced　hypertension　and　vascular　remodeling　in　WT　mice　were　attenuated　in　NLRP3(-/-)　mice.　Furthermore,　Ang　IIinduced　NLRP3　inflammasome　activation,　phenotypic　transformation　and　proliferating　cell　nuclear　antigen　(PCNA)　upregulation　were　inhibited　in　the　media　of　aorta　of　NLRP3(-/-)　mice.　Conclusions:　NLRP3　inflammasome　activation　contributes　to　Ang　IIinduced　VSMC　phenotypic　transformation　and　proliferation　as　well　as　vascular　remodeling　and　hypertension.　(C)　2017　The　Author(s)　Published　by　S.　Karger　AG,　Basel