尾加压素Ⅱ的促丝裂作用

为研究体内新发现的缩血管活性肽尾加压素Ⅱ对细胞的促丝裂作用，在培养的大鼠动脉血管平滑肌细胞和气道平滑肌细胞、心肌成纤维细胞以及肾系膜细胞上，采用^3H－胸腺嘧啶掺入法，观察了尾加压素Ⅱ对细胞DNA合成影响。结果显示尾加压素Ⅱ明显促进细胞^3H－胸腺嘧啶掺入增加，并在一定浓度范围内呈剂量依赖性。但同一剂量的尾加压素Ⅱ在不同细胞产生的作用强弱不同，10^-10mol/L的尾加压素Ⅱ公对心肌成纤维细胞和气道平滑肌细胞有刺激作用，且成纤维细胞＞气道平滑肌细胞，10^-9-10^-8mol/L尾加压素Ⅱ对诸细胞的效应则为心肌成纤维细胞＞气道平滑肌细胞＞肾系膜细胞＞血管平滑肌细胞，而高浓度尾加压素Ⅱ（10^-7mol/L）对心肌成纤维细胞增殖的刺激作用明显减弱。这些结果提示尾加压素Ⅱ是一种新发现的内源性丝裂原，其促丝裂效应在疾病发生中的作用值得进一步研究。

Mitogenic Effect of Urotensin

Aim To investigate the mitogenic effect of urotensin II oncells. Methods In cultured rat aorta smooth muscle cells (VSMC), tracheal smooth muscle cells (TSMC), cardiac fibroblasts (CF) and glomerular mesagial cells (GMC), UⅡ was used to stimulate these cells and levels of 3 H-TdR incorporation were used to evaluate the speed of DNA synthesis. Results UⅡ increased levels in concentration-dependent manner of 3 H-TdR incorporation of these cells significantly. But in different cells, UⅡ of same concentration did not induce same effect. 10-10 mol/L UⅡ could increase levels of 3 H-TdR incorporation of CF and TSMC only, with the incorporation of CF higher than TSMC, while 10-9～10-8 mol/L UⅡ induced effect in the following order:CF>TSMC>GMC>VSMC. However, 10-6～10-7mol/L UⅡ showed weaker stimulating effects on CF than lower concentration of UⅡ(10-10～10-8 mol/L)． Conclusion These study provides evidence that urotensin II is an endogenous mitogen for some cells and the contribution of mitogenic effect of UⅡ to diseases deserves investigating greatly.