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目的研究体内新发现的缩血管活性肽尾加压素Ⅱ（ｕｒｏｔｅｎｓｉｎ Ⅱ， Ｕ Ⅱ）对大鼠主动脉平滑肌细胞增殖作用的影响以及ＵⅡ作用的细胞内信号转导机制。方法在培养的大鼠主动脉平滑肌细胞（ＡＳＭＣ）上，采用［３Ｈ］－胸腺嘧啶（［３Ｈ］－ＴｄＲ）参入法，观察 ＵⅡ对细胞 ＤＮＡ合成的刺激作用；加入不同的细胞内信号转导阻断剂，观察对ＵⅡ效应的影响。结果 Ｉ× １０－９～ １× １０－７ ｍｏｌ·Ｌ－１ ＵⅡ以浓度依赖方式促进 ＡＳＭＣ［３Ｈ］－ＴｄＲ参入增加， １× １０－９、１× １０－８和 １×１０－７ｍｏｌ·Ｌ－１ＵⅡ组［３Ｈ］－ＴｄＲ参入量分别较对照组增加２２％（Ｐ＜０．０５），５７％（Ｐ＜０，０１）和６５％（Ｐ＜０．０１）。ＵⅡ的效应能被钙通道阻断剂尼卡地平、ＰＫＣ阻断剂Ｈ７、钙调素激酶（ＣａＭ－ＰＫ）阻断剂 Ｗ７和 ＭＡＰＫ阻断剂 ＰＤ９８０５９所阻断，抑制率分别为５５％（Ｐ＜０．０１），２７％（Ｐ＜０．０１），１８％（Ｐ＜０．０５）和１６％（Ｐ＜０．０５）。结论 ＵⅡ是一种新发现的强烈的促ＡＳＭＣ增生的内源性丝裂原，其促丝裂效应可能通过Ｃａ２＋、ＰＫＣ、ＣａＭ－ＰＫ和ＭＡＰＫ来介导。
Objective To investigate the effect of urotensin Ⅱ (UⅡ), a newly discovered vasoconstrictor, on the proliferation of rat aortic smooth muscle cells and the intracellular signal transduction mechanism of UⅡ. Methods [3H] thymidine ([3H] -TdR) was used to observe the stimulatory effect of UⅡ on DNA synthesis in cultured rat aortic smooth muscle cells (ASMCs). Different intracellular signal transduction Blockers, observed on the U Ⅱ effect. Results I × 10-9 ~ 1 × 10-7 mol·L-1 UⅡ promoted ASMC [3H] -TdR incorporation, 1 × 10-9, 1 × 10-8, and 1 × 10-7 mol·L-1 in a concentration-dependent manner The incorporation of [3H] -TdR in L-1UⅡgroup increased by 22% (P <0.05), 57% (P <0,01) and 65% (P <0.01) compared with the control group respectively. The effect of UII was blocked by nicorandipine, PKC blocker H7, CaM-PK blocker W7 and MAPK blocker PD98059 with the inhibitory rates of 55% ( P <0.01), 27% (P <0.01), 18% (P <0.05) and 16% (P <0.05) respectively. Conclusion UⅡ is a newly discovered endogenous mitogen that promotes proliferation of ASMC. Its mitogenic effect may be mediated by Ca2 +, PKC, CaM-PK and MAPK.