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Long non-coding RNAs (lncRNAs) play key roles in Angiotensin II (AngII) signaling but their role in chondrogenic transformation of vascular smooth muscle cells (VSMCs) is unknown. We describe a novel AngII-induced lncRNA <i>Alivec</i> (Angiotensin II-induced lncRNA in VSMCs eliciting chondrogenic phenotype) implicated in VSMC chondrogenesis. In rat VSMCs, <i>Alivec</i> and the nearby gene <i>Acan</i>, a chondrogenic marker, were induced by growth factors AngII and PDGF and the inflammatory cytokine TNF-α. AngII co-regulated <i>Alivec</i> and <i>Acan</i> through the activation of AngII type1 receptor signaling and Sox9, a master transcriptional regulator of chondrogenesis. <i>Alivec</i> knockdown with GapmeR antisense-oligonucleotides attenuated the expression of AngII-induced chondrogenic marker genes, including <i>Acan</i>, and inhibited the chondrogenic phenotype of VSMCs. Conversely, <i>Alivec</i> overexpression upregulated these genes and promoted chondrogenic transformation. RNA-pulldown coupled to mass-spectrometry identified Tropomyosin-3-alpha and hnRNPA2B1 proteins as <i>Alivec</i>-binding proteins in VSMCs. Furthermore, male rats with AngII-driven hypertension showed increased aortic expression of <i>Alivec</i> and <i>Acan</i>. A putative human ortholog <i>ALIVEC</i>, was induced by AngII in human VSMCs, and this locus was found to harbor the quantitative trait loci affecting blood pressure. Together, these findings suggest that AngII-regulated lncRNA <i>Alivec</i> functions, at least in part, to mediate the AngII-induced chondrogenic transformation of VSMCs implicated in vascular dysfunction and hypertension.