SUMMARY Objective: To investigate the role of calcium signal in the
proliferation of vascular smooth muscle cells (VSMC)
induced by
Urotensin Ⅱ (UⅡ). Methods: The effect of UⅡ on the
proliferation of VSMC was measured by 3H TdR incorporation and Flowcytometry method. The action of UⅡ on the 45 Ca 2+ uptake of rat aorta medium membrane was estimated in vitro . Technique of Laser Scanning Confocal Microscope (LSCM) was used to monitor the change of Ca 2+ in the cytoplasm induced by UⅡ.Results: UⅡ (10 -9 ～10 -7 mol·L -1 ) increased the DNA synthesis of VSMC and promoted the transformation of the cells from resting state to a proliferative one in a concentration dependent manner. UⅡ (10 -8 mol·L -1 ) increased the Proliferation Index
by 192% as compared with the control. Nicardipine, a calcium channel blocker, and EDTA, a calcium chelate agent, both significantly inhibited the UⅡ induced proliferation of VSMC. After incubation of VSMC with both nicardipine(10 -5 mol·L -1 ) and UⅡ(10 -8 mol·L -1 ), the DNA synthesis in VSMC was only 59.0% of that in the UⅡ(10 -8 mol·L -1 ) alone group. UⅡ stimulated 45 Ca 2+ uptake of aorta was increased in a concentration dependent manner, which was significantly inhibited by pretreatment with nicardipine. UⅡ produced a rapid increase in cytoplasmic Ca 2+ concentration and the Ca 2+ wave persisted about 3 min. Conclusion: UⅡ promotes the proliferation of VSMC through stimulating the Ca 2+ uptake from extracellular calcium and increasing cytoplasmic Ca 2+ concentration