Aim Hypertension-induced cardiovascular remodeling is associated with abnormally increased biomechanical stress.To explore how the cardiovascular cells sense and convert the extracellular mechanical stress into intracellular biochemical signals leading to finally pathophysiological responses.Methods When rat vascular smooth muscle cells cultivated on a flexible membrane were subjected to cyclic strain stress(60 cycles/min,15% elongation) at various time points,translocation and phosphorylation of protein kinase C(PKC)βⅡ were observed as detected by Western blot analysis.In addition,the stretched vascular smooth muscle cells were labeled using ~3H-thymidine for 6h and then harvested for ~3H-thymidine-labeled cell count.Results Equal distribution of PKCβⅡ was observed in cytosole and membrane of the quiescent vascular smooth muscle cells,respectively.While vascular smooth muscle cells were subjected to mechanical stress,induction of translocation of PKCβⅡ was observed as distributed by 20.9% in the cytosole and 79.1% in the membrane,implying that mechanical stress induced PKCβⅡ translocation from cytosole to membrane.Concomitantly,mechanical forces evoked rapid activation of PKCβⅡ in a time dependent manner showing that phosphorylation of PKCβⅡ peaked at 2min and declined after then in response to mechanical stress,while no phosphorylation of PKCβⅡ occurred in the untreated cells.In addition,mechanical forces significantly induced increase of DNA synthesis of vascular smooth muscle cells as demonstrated by incorporation of -thymidine compared to no treated cells.Conclusion Mechanical stress significantly induced translocation and phosphorylation of PKCβⅡ in the vascular smooth muscle cells leading to increased vascular smooth muscle cell proliferation.This data will be useful for understanding the molecular mechanisms of hypertension and its related cardiovascular diseases,and providing approaches of prevention and treatment of this disease.